☆ 4.7 Review

Doxorubicin-mediated cardiac dysfunction: Revisiting molecular interactions, pharmacological compounds and (nano)theranostic platforms

ENVIRONMENTAL RESEARCH (2023)

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Review Pharmacology & Pharmacy

Silymarin as a preventive or therapeutic measure for chemotherapy and radiotherapy-induced adverse reactions: a comprehensive review of preclinical and clinical data

Mahsa Ghodousi et al.

Summary: This review examines the use of silymarin in preventing or treating adverse reactions caused by chemotherapy or radiotherapy. Results show that silymarin has various protective effects, including antioxidative, anti-apoptotic, anti-inflammatory, and anti-immunomodulatory properties, effectively managing multiple adverse reactions. Clinical trials suggest that oral silymarin may be a promising adjuvant in cancer treatment, particularly against hepatotoxicity, nephrotoxicity, diarrhea, and mucositis. Topical formulations of silymarin are also effective against radiodermatitis and hand-foot syndrome.

EUROPEAN JOURNAL OF CLINICAL PHARMACOLOGY (2023)

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Review Pharmacology & Pharmacy

Critical design parameters to develop biomimetic organ-on-a-chip models for the evaluation of the safety and efficacy of nanoparticles

Mahmoud Abdelkarim et al.

Summary: Organ-on-a-chip (OOC) models, based on microfluidics, can replicate the microstructure of organs and tissues and the dynamic microenvironment inside the human body. This review discusses the impact of different design parameters on the performance of OOC models and explores how mechanical forces affect the transport of nanoparticles (NPs) across biological barriers, cell uptake, and biocompatibility.

EXPERT OPINION ON DRUG DELIVERY (2023)

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Article Cardiac & Cardiovascular Systems

Thioredoxin Reductase 2 Synergizes with Cytochrome c, Somatic to Alleviate Doxorubicin-Induced Oxidative Stress in Cardiomyocytes and Mouse Myocardium

Chuyun Li et al.

Summary: The study aimed to investigate the impact of thioredoxin reductase 2 (TXNRD2) and cytochrome c, somatic (CYCS) on doxorubicin (DOX)-induced oxidative stress (OS) in cardiomyocytes and mouse myocardium. TXNRD2 and CYCS were found to be downregulated in DOX-treated cardiomyocytes and mice. Overexpression of TXNRD2 or CYCS enhanced cell viability, reduced oxidative stress levels, and improved cardiac pathologic changes and function.

INTERNATIONAL HEART JOURNAL (2023)

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Article Immunology

Therapeutic treatment with phosphodiesterase-4 inhibitors alleviates kidney injury and renal fibrosis by increasing MMP-9 in a doxorubicin-induced nephrotoxicity mouse model

Walyson Coelho Costa et al.

Summary: The effects of PDE-4 inhibitors rolipram and roflumilast on a doxorubicin-induced nephrotic syndrome model were evaluated. The results showed that early-stage rolipram treatment preserved glomerular filtration barrier function and reduced inflammation and renal fibrosis. Late-stage treatment with either rolipram or roflumilast also protected glomerular filtration barrier function and reduced renal tissue fibrosis.

INTERNATIONAL IMMUNOPHARMACOLOGY (2023)

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Article Biochemistry & Molecular Biology

MicroRNAs target the PI3K/Akt/p53 and the Sirt1/Nrf2 signaling pathways in doxorubicin-induced cardiotoxicity

Fatemeh Yarmohammadi et al.

Summary: This manuscript reviews the regulation of the PI3K/Akt/p53 and the Sirt1/Nrf2 pathways by miRNAs in DOX-induced cardiotoxicity.

JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY (2023)

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Article Pharmacology & Pharmacy

Doxorubicin-induced acute cardiotoxicity is associated with increased oxidative stress, autophagy, and inflammation in a murine model

Patricia Lorena Dulf et al.

NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY (2023)

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Article Cell Biology

Tubeimoside I Ameliorates Doxorubicin-Induced Cardiotoxicity by Upregulating SIRT3

Wei Zhang et al.

Summary: Tubeimoside I (TBM) can alleviate doxorubicin (DOX)-induced cardiotoxicity by increasing the expression of SIRT3, thereby reducing inflammation, oxidative stress, and cardiomyocyte apoptosis.

OXIDATIVE MEDICINE AND CELLULAR LONGEVITY (2023)

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Article Pharmacology & Pharmacy

Protective role of cezanne in doxorubicin-induced cardiotoxicity by inhibiting autophagy, apoptosis and oxidative stress

Jiayan Zhang et al.

Summary: Doxorubicin (DOX) is commonly used in clinical practice but its benefits are limited by complications such as excessive apoptosis and autophagy, overproduction of reactive oxygen species (ROS), and oxidative stress. This study found that the protein OTUD7B (Cezanne) plays a role in DOX-induced cardiotoxicity. Overexpression of Cezanne can alleviate DOX-induced cardiomyocyte apoptosis, autophagy, and oxidative stress by activating the PI3K/AKT/mTOR pathway.

TOXICOLOGY (2023)

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Article Biochemistry & Molecular Biology

Daidzein ameliorates doxorubicin-induced cardiac injury by inhibiting autophagy and apoptosis in rats

Jinxia Wu et al.

Summary: Daidzein can protect the heart from Doxorubicin-induced cardiotoxicity by inhibiting the PI3K/Akt pathway, thereby reducing autophagy and apoptosis.

FOOD & FUNCTION (2023)

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Review Pharmacology & Pharmacy

Acoustically-Activated Liposomal Nanocarriers to Mitigate the Side Effects of Conventional Chemotherapy with a Focus on Emulsion-Liposomes

Mah Noor Zafar et al.

Summary: In order to improve current cancer treatments, nanomaterials are used as smart drug delivery vehicles that can be designed to specifically target cancer cells and respond to stimulation. These nanocarriers can encapsulate chemotherapy drugs and deliver them to the affected area, reducing the side effects associated with conventional systemic administration. Different sonosensitive liposomal formulations that can be stimulated using acoustic methods are discussed in this review. Emulsion liposomes (eLiposomes) are highlighted for their ability to promote drug release at low intensities and short exposure times compared to regular liposomes. Other formulations incorporating microbubbles and nanobubbles are also explored.

PHARMACEUTICS (2023)

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Article Medicine, Research & Experimental

Melatonin alleviates doxorubicin-induced cardiotoxicity via inhibiting oxidative stress, pyroptosis and apoptosis by activating Sirt1/Nrf2 pathway

Wei Zhang et al.

Summary: Melatonin has cardioprotective effects on various cardiovascular diseases, including doxorubicin-induced cardiomyopathy. It has been shown to enhance mitochondrial function and mitigate myocardial injuries caused by Doxorubicin, but its role in regulating the Sirt1/Nrf2 pathway in lessening the onset of cardiomyopathy is still unclear.

BIOMEDICINE & PHARMACOTHERAPY (2023)

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Article Cardiac & Cardiovascular Systems

Metformin and Dapagliflozin Attenuate Doxorubicin-Induced Acute Cardiotoxicity in Wistar Rats: An Electrocardiographic, Biochemical, and Histopathological Approach

Shakta Mani Satyam et al.

Summary: This study aimed to investigate the cardioprotective potential of metformin and dapagliflozin against doxorubicin-induced acute cardiotoxicity. It was found that both metformin and dapagliflozin can alleviate doxorubicin-induced cardiac injury and improve blood biochemical markers, as demonstrated by ECG and blood testing in rats.

CARDIOVASCULAR TOXICOLOGY (2023)

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Article Environmental Sciences

3,4-benzopyrene aggravates myocardial ischemia-reperfusion injury-induced pyroptosis through inhibition of autophagy-dependent NLRP3 degradation

Kai-Yu Huang et al.

Summary: Polycyclic aromatic hydrocarbons (PAHs) are widely present in the environment and are produced during combustion of organic matter. This study investigated the effect of 3,4-benzo[a]pyrene (BaP), a commonly studied PAH, on myocardial ischemia-reperfusion (I/R) injury. The results showed that BaP aggravated myocardial pyroptosis in an autophagy-dependent manner and activated the p53-BNIP3 pathway to decrease autophagosome clearance. These findings provide new insights into the mechanisms of cardiotoxicity and suggest the p53-BNIP3 pathway as a potential therapeutic target for BaP-induced myocardial I/R injury.

ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY (2023)

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Article Environmental Sciences

Naringin against doxorubicin-induced hepatotoxicity in mice through reducing oxidative stress, inflammation, and apoptosis via the up-regulation of SIRT1

Yan Xi et al.

Summary: This study showed that naringin had protective effects on doxorubicin-induced liver injury by reducing cell injury, reactive oxygen species release, apoptosis level, and by decreasing aspartate transaminase, alanine transaminase, and malondialdehyde levels, and increasing superoxide dismutase, glutathione, and catalase levels. These effects were mediated by up-regulation of SIRT1 and inhibition of downstream inflammatory, apoptotic, and oxidative stress signaling pathways. Naringin is a valuable compound for preventing doxorubicin-induced liver damage.

ENVIRONMENTAL TOXICOLOGY (2023)

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Article Medicine, Research & Experimental

Cardiac-specific overexpression of catalase attenuates lipopolysaccharide-induced cardiac anomalies through reconciliation of autophagy and ferroptosis

Hu Peng et al.

Summary: This study aimed to investigate the effect of the antioxidant enzyme catalase on LPS-induced cardiac abnormalities and the mechanisms involved, with particular focus on the interplay between autophagy, ferroptosis, and apoptosis. The results showed that catalase can alleviate the inhibitory effect of LPS on cardiac function and improve adverse effects such as cardiac fibrosis.

LIFE SCIENCES (2023)

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Review Chemistry, Medicinal

The role and prospect of lysine-specific demethylases in cancer chemoresistance

Ying-Qi Song et al.

Summary: Histone methylation is involved in regulating gene expression and maintaining genome integrity and epigenetic inheritance. Abnormalities in histone methylation are commonly observed in human diseases, especially cancer. Lysine demethylases (KDMs) can reverse lysine methylation mediated by histone methyltransferases. KDMs play a role in drug resistance by altering the metabolic profile of cancer cells, upregulating cancer stem cells and drug-tolerant genes, and promoting the epithelial-mesenchymal transition and metastatic ability. This review discusses the structural features and functions of KDMs, their preferences in different cancers, and the mechanisms of drug resistance resulting from KDMs. It also explores KDM inhibitors used to combat drug resistance in cancer and the opportunities and challenges of targeting KDMs for cancer therapy.

MEDICINAL RESEARCH REVIEWS (2023)

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Article Neurosciences

Curcumin protects against doxorubicin induced oxidative stress by regulating the Keap1-Nrf2-ARE and autophagy signaling pathways

Dehua Liao et al.

Summary: Doxorubicin-induced neurotoxicity has been widely reported, and oxidative stress plays a critical role in this process. Curcumin has been shown to alleviate depressive-like state by mitigating oxidative stress and activating Nrf2-ARE signaling pathway. However, the exact mechanism of Curcumin in alleviating Doxorubicin-induced neurotoxicity is still unknown.

PSYCHOPHARMACOLOGY (2023)

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Review Nutrition & Dietetics

p53 at the Crossroads between Doxorubicin-Induced Cardiotoxicity and Resistance: A Nutritional Balancing Act

Yuanfang Guo et al.

Summary: Doxorubicin is an effective chemotherapy drug, but it can cause cardiotoxicity and drug resistance. p53 mutation or inactivation is a primary cause of DOX resistance. Although p53 suppression can reduce DOX-induced cardiotoxicity, it conflicts with the antitumor advantages of p53 reactivation. Therefore, exploring p53-targeted anticancer strategies is crucial to enhance the effectiveness of DOX.

NUTRIENTS (2023)

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Review Biochemistry & Molecular Biology

MicroRNA in the Diagnosis and Treatment of Doxorubicin-Induced Cardiotoxicity

Ziyu Kuang et al.

Summary: Doxorubicin (DOX) is a widely used chemotherapy drug for cancer treatment; however, its clinical utility is limited due to DOX-induced cardiotoxicity (DIC). Conventional detection methods are ineffective in early monitoring and detecting DIC. Therefore, there is a need for sensitive, accurate, and specific diagnostic and treatment methods. MicroRNAs (miRNAs) have been identified as stable and detectable molecules and are being studied as potential biomarkers and therapeutic targets for DIC. This review summarizes the current research on the diagnosis and treatment of miRNAs in DIC, discusses the feasibility and challenges of using miRNAs as diagnostic biomarkers and therapeutic targets, and provides recommendations for future studies.

BIOMOLECULES (2023)

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Article Biochemistry & Molecular Biology

Monotropein attenuates doxorubicin-induced oxidative stress, inflammation, and arrhythmia via the AKT signal pathway

Zhao Fang et al.

Summary: As a glycoside iridoid, monotropein (MON) has various pharmacological properties, including anti-inflammatory, antioxidant, and anti-apoptotic effects. This study aimed to investigate the role of MON in doxorubicin (DOX)-induced cardiotoxicity. The results showed that MON treatment reduced DOX-induced myocardial damage, improved cardiac dysfunction, and reversed inflammation, oxidative stress, and ventricular fibrillation risk. It was also found that MON activated the AKT signaling pathway to exert its cardioprotective effects.

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS (2023)

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Article Biochemistry & Molecular Biology

Scutellarin Attenuates Doxorubicin-Induced Cardiotoxicity by Inhibiting Myocardial Fibrosis, Apoptosis and Autophagy in Rats

Xipeng Sun et al.

Summary: This study found that scutellarin has a protective effect against chronic cardiotoxicity induced by doxorubicin, possibly by reducing oxidative stress, myocardial fibrosis, apoptosis, and autophagy.

CHEMISTRY & BIODIVERSITY (2023)

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Article Multidisciplinary Sciences

Apigenin-coated gold nanoparticles as a cardioprotective strategy against doxorubicin-induced cardiotoxicity in male rats via reducing apoptosis

Zeynab Sharifiaghdam et al.

Summary: This study investigated the cardioprotective effects of apigenin synthesized gold nanoparticles (Api-AuNPs) in doxorubicin-induced cardiotoxicity (DIC). The results showed that Api-AuNPs treatment significantly reduced body and heart weight loss caused by DOX, and decreased the levels of injury markers. Moreover, Api-AuNPs ameliorated tissue damage by regulating the expression of Bax, caspase3, and Bcl-2, thus exerting anti-apoptotic effects on cardiomyocytes.

HELIYON (2023)

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Article Biochemistry & Molecular Biology

Carnosic acid protects against doxorubicin-induced cardiotoxicity through enhancing the Nrf2/HO-1 pathway

Shan Hu et al.

Summary: A study found that carnosic acid (CA) can inhibit the oxidative damage, apoptosis, and pyroptosis induced by doxorubicin (DOX) in the heart, thereby protecting the heart. This study suggests that CA could be a potential therapeutic strategy in the prevention of DOX-associated cardiomyopathy.

FOOD & FUNCTION (2023)

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Article Nutrition & Dietetics

Biomimetic Nanozymes Suppressed Ferroptosis to Ameliorate Doxorubicin-Induced Cardiotoxicity via Synergetic Effect of Antioxidant Stress and GPX4 Restoration

Yunpeng Zhang et al.

Summary: This study evaluated the role of cerium oxide-based nanozymes in preventing and treating doxorubicin-induced cardiotoxicity. The nanoparticles showed excellent antioxidant response and bioregulation, effectively reversing myocardial remodeling and reducing myocardial necrosis. The study suggests that cerium oxide-based nanozymes could be a promising candidate for the prevention and treatment of doxorubicin-induced cardiotoxicity.

NUTRIENTS (2023)

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Article Chemistry, Multidisciplinary

Montelukast ameliorates doxorubicin-induced cardiotoxicity via modulation of p-glycoprotein and inhibition of ROS-mediated TNF-α/NF-κB pathways

Heba M. Hafez et al.

Summary: This study found that montelukast (ML) has a protective effect against doxorubicin (DOX)-induced cardiotoxicity. ML improved cardiac enzymes, reduced oxidative stress and inflammation, and enhanced P-glycoprotein (P-gp) activity, suggesting its potential as a cardioprotective adjuvant during DOX use.

DRUG AND CHEMICAL TOXICOLOGY (2022)

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Article Pharmacology & Pharmacy

A Combination of Virgin Coconut Oil and Extra Virgin Olive Oil Elicits Superior Protection Against Doxorubicin Cardiotoxicity in Rats

Andi Ulfiana Utari et al.

Summary: Combining VCO and EVOO was found to be more effective in protecting against DOX-induced cardiotoxicity in rats compared to their individual use.

TURKISH JOURNAL OF PHARMACEUTICAL SCIENCES (2022)

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Article Biochemistry & Molecular Biology

Melatonin ameliorates trimethyltin chloride-induced cardiotoxicity: The role of nuclear xenobiotic metabolism and Keap1-Nrf2/ARE axis-mediated pyroptosis

Jingzeng Cai et al.

Summary: TMT induces cardiac damage, inflammation, and oxidative stress, while MT mitigates these adverse changes.

BIOFACTORS (2022)

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Article Cardiac & Cardiovascular Systems

Protective Effect of Qiliqiangxin against Doxorubicin-Induced Cardiomyopathy by Suppressing Excessive Autophagy and Apoptosis

Yating Qin et al.

Summary: In this study, it was found that Qiliqiangxin (QL), a traditional Chinese medicine formulation, exhibited protective effects against doxorubicin (DOX)-induced cardiotoxicity. The underlying mechanisms may involve the inhibition of autophagy and apoptosis activities, as well as the regulation of the PI3K/AKT/mTOR pathway.

CARDIOVASCULAR THERAPEUTICS (2022)

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Article Cardiac & Cardiovascular Systems

Curcumin Ameliorates Doxorubicin-Induced Cardiotoxicity and Hepatotoxicity Via Suppressing Oxidative Stress and Modulating iNOS, NF-κB, and TNF-α in Rats

Ghadha Ibrahim Fouad et al.

Summary: This study demonstrates that curcumin has protective effects against DOX-induced cardiotoxicity and hepatotoxicity by reducing inflammation and oxidative stress in cardiac and hepatic tissues. Curcumin can also restore tissue structure and decrease blood-based biomarkers cTn1, IFN-gamma, and AST to provide cardioprotection and hepatoprotection.

CARDIOVASCULAR TOXICOLOGY (2022)

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Article Cell Biology

MicroRNA-495-3p diminishes doxorubicin-induced cardiotoxicity through activating AKT

Jun Meng et al.

Summary: miR-495-3p protects against Dox-induced cardiotoxicity by activating the AKT pathway.

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE (2022)

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Review Biochemistry & Molecular Biology

The Role of Flavonoids as a Cardioprotective Strategy against Doxorubicin-Induced Cardiotoxicity: A Review

Rony Abdi Syahputra et al.

Summary: Doxorubicin is a widely used anticancer drug, but its therapeutic value is hindered by dose-dependent cardiotoxicity. This review summarizes the cardioprotective effects of flavonoids against doxorubicin-induced cardiac toxicity in both in vitro and in vivo models.

MOLECULES (2022)

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Article Biochemistry & Molecular Biology

Potential Protective Effect of Coenzyme Q10 on Doxorubicin-Induced Neurotoxicity and Behavioral Disturbances in Rats

Nilsel Okudan et al.

Summary: The aim of this study was to investigate the potential neuroprotective efficacy of coenzyme Q10 (CoQ10) against doxorubicin (DOX)-induced behavioral disturbances in rats. The results showed that CoQ10 significantly attenuated DOX-induced behavioral alterations by improving acetylcholinesterase (AChE) activity in the brain tissue.

NEUROCHEMICAL RESEARCH (2022)

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Article Plant Sciences

Apocynum venetum leaf extract alleviated doxorubicin-induced cardiotoxicity through the AKT/Bcl-2 signaling pathway

Yang Zhang et al.

Summary: Apocynum venetum L. leaf extract alleviates doxorubicin-induced cardiomyocyte apoptosis by suppressing oxidative stress and apoptosis through the AKT/Bcl-2 signaling pathway.

PHYTOMEDICINE (2022)

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Review Chemistry, Medicinal

Curcumin and its derivatives in cancer therapy: Potentiating antitumor activity of cisplatin and reducing side effects

Asal Jalal Abadi et al.

Summary: Curcumin, isolated from Curcuma longa, has potent tumor-suppressor activity and can decrease the adverse impacts of cisplatin (CP) while enhancing its antitumor activity. Curcumin reduces ROS levels to prevent apoptosis in normal cells, inhibits inflammation, and reduces various toxicities caused by CP. Additionally, curcumin potentiates CP cytotoxicity and suppresses tumor-promoting pathways to prevent drug resistance.

PHYTOTHERAPY RESEARCH (2022)

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Article Pharmacology & Pharmacy

Melatonin alleviates doxorubicin-induced mitochondrial oxidative damage and ferroptosis in cardiomyocytes by regulating YAP expression

Xiao Sun et al.

Summary: This study investigates the protective effects of melatonin against doxorubicin-induced cardiotoxicity, and reveals its involvement in modulating ferroptosis and YAP expression. These findings provide insights into potential therapeutic strategies for ameliorating doxorubicin-induced cardiotoxicity.

TOXICOLOGY AND APPLIED PHARMACOLOGY (2022)

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Article Chemistry, Multidisciplinary

Mollification of Doxorubicin (DOX)-Mediated Cardiotoxicity Using Conjugated Chitosan Nanoparticles with Supplementation of Propionic Acid

Durairaj Siva et al.

Summary: This study investigates the possible mechanism of doxorubicin-mediated cardiotoxicity and explores the use of chitosan nanoparticles conjugated with doxorubicin and supplemented with propionic acid to reduce the cardiotoxicity. The results show that DCNPs and propionic acid have a protective effect against doxorubicin-induced cardiotoxicity.

NANOMATERIALS (2022)

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Article Biotechnology & Applied Microbiology

Lapatinib induces mitochondrial dysfunction to enhance oxidative stress and ferroptosis in doxorubicin-induced cardiomyocytes via inhibition of PI3K/AKT signaling pathway

Lei Sun et al.

Summary: This study aimed to explore the mechanism involved in the synergistic effect of lapatinib (LAP) in doxorubicin (DOX)-induced cardiotoxicity. The results showed that LAP aggravated cell injury, apoptosis, and mitochondrial dysfunction induced by DOX. Additionally, LAP in combination with DOX induced oxidative stress and ferroptosis. The activation of PI3K/AKT signaling reversed the detrimental effects of LAP on DOX-induced cardiotoxicity.

BIOENGINEERED (2022)

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Article Biochemistry & Molecular Biology

RRM2 Alleviates Doxorubicin-Induced Cardiotoxicity through the AKT/mTOR Signaling Pathway

Yuheng Jiao et al.

Summary: This study aimed to investigate the role and mechanism of ribonucleotide reductase M2 subunit (RRM2) in doxorubicin (DOX)-induced cardiotoxicity. The results showed that reduced expression of RRM2 led to increased apoptosis and autophagy in DOX-treated cardiomyocytes. On the contrary, RRM2 overexpression alleviated DOX-induced cardiotoxicity. Mechanistically, RRM2 could regulate DOX-induced cardiotoxicity through the AKT/mTOR signaling pathway.

BIOMOLECULES (2022)

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Article Medicine, Research & Experimental

MiR-24-3p Attenuates Doxorubicin-induced Cardiotoxicity via the Nrf2 Pathway in Mice

Di Fan et al.

Summary: miR-24-3p protects cardiomyocytes against DOX-induced heart injury by activating the Nrf2 pathway and reducing oxidative stress and cell loss.

CURRENT MEDICAL SCIENCE (2022)

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Article Pharmacology & Pharmacy

Curcumin-coated gold nanoparticles attenuate doxorubicin-induced cardiotoxicity via regulating apoptosis in a mouse model

Zeynab Sharifiaghdam et al.

Summary: This study synthesized gold nanoparticles based on Cur (Cur-AuNPs) and found that the cardioprotective effect of Cur-AuNPs was more effective than Cur alone in a DOX-induced cardiotoxic mouse model, as evidenced by reductions in cardiac injury biomarkers and apoptotic proteins, as well as an increase in anti-apoptotic proteins. The results were observed both in short-term (24 hours) and long-term (14 days) studies.

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY (2022)

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Article Toxicology

Dapagliflozin protects against doxorubicin-induced cardiotoxicity by restoring STAT3

Wei-Ting Chang et al.

Summary: This study found that DAPA has a protective effect against Dox-induced cardiotoxicity and demonstrated the important role of STAT3 in this process. DAPA improves cardiac function by reducing cardiac fibrosis and inhibiting cell apoptosis and reactive oxygen species generation. Furthermore, the study also showed that DAPA can restore Dox-suppressed STAT3 expression.

ARCHIVES OF TOXICOLOGY (2022)

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Article Biochemistry & Molecular Biology

Targeted regulation of autophagy using nanoparticles: New insight into cancer therapy

Mahshid Deldar Abad Paskeh et al.

Summary: Autophagy plays a dual role in normal cells and tumors, and targeting autophagy using nanoparticles can enhance cancer therapy. Nanocarriers can deliver autophagy regulators and chemotherapeutic agents, while nanomaterials can affect key components of autophagy.

BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE (2022)

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Article Cardiac & Cardiovascular Systems

SIRT1 in the cardiomyocyte counteracts doxorubicin-induced cardiotoxicity via regulating histone H2AX

Atsushi Kuno et al.

Summary: The study suggests that SIRT1 protects against doxorubicin-induced cardiotoxicity by mediating H2AX phosphorylation through its deacetylation in cardiomyocytes. Treatment with resveratrol, a SIRT1 activator, attenuates doxorubicin-induced cardiac dysfunction by reducing the acetyl-Lys5-H2AX level and preserving the phospho-Ser139-H2AX level.

CARDIOVASCULAR RESEARCH (2022)

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Article Cardiac & Cardiovascular Systems

Protective Effect of Curcumin, Chrysin and Thymoquinone Injection on Trastuzumab-Induced Cardiotoxicity via Mitochondrial Protection

Leila Rezaie Shirmard et al.

Summary: This study aimed to evaluate the mitochondrial protective effects of curcumin, chrysin, and thymoquinone against trastuzumab-induced cardiotoxicity. The results showed that curcumin, chrysin, and thymoquinone could attenuate cardiac mitochondrial impairments and histopathological alterations caused by trastuzumab. These protective effects may be attributed to their antioxidant and mitochondrial protection activities.

CARDIOVASCULAR TOXICOLOGY (2022)

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Article Biochemistry & Molecular Biology

Simultaneous proteasome and autophagy inhibition synergistically enhances cytotoxicity of doxorubicin in breast cancer cells

Jian Sheng Loh et al.

Summary: In this study, it was found that the combination of doxorubicin and ixazomib induced autophagy in breast cancer cells, which had a cytoprotective role. Simultaneous inhibition of the ubiquitin-proteasome system and autophagy enhanced the cytotoxicity of doxorubicin.

CELL BIOCHEMISTRY AND FUNCTION (2022)

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Article Biochemistry & Molecular Biology

PRMT4 promotes ferroptosis to aggravate doxorubicin-induced cardiomyopathy via inhibition of the Nrf2/GPX4 pathway

Yilong Wang et al.

Summary: PRMT4 promotes ferroptosis in DOX-induced cardiomyocyte ferroptosis by interacting with Nrf2 and inhibiting its nuclear translocation, which subsequently suppresses the transcription of GPX4. Activation of Nrf2 or administration of Fer-1 abolishes the detrimental role of PRMT4 in DOX-induced cardiomyocyte ferroptosis.

CELL DEATH AND DIFFERENTIATION (2022)

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Article Cell Biology

Ginsenoside Rh2 mitigates doxorubicin-induced cardiotoxicity by inhibiting apoptotic and inflammatory damage and weakening pathological remodelling in breast cancer-bearing mice

Jingang Hou et al.

Summary: The study found that ginsenoside Rh2 can reduce the cardiotoxicity caused by doxorubicin (Dox) by inhibiting cardiac histopathological changes, apoptosis, necrosis, and inflammation. Rh2 also attenuates pathological remodeling by reducing fibroblast to myofibroblast transition (FMT) and endothelial-mesenchymal transition (EndMT). RNA-sequencing analysis showed that Dox treatment predominantly targets cell cycle and microtubule attachment, while Rh2 regulates these effects. Interestingly, Rh2 also attenuates fibrosis by promoting senescence in myofibroblasts and reversing established myofibroblast differentiation in EndMT.

CELL PROLIFERATION (2022)

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Article Environmental Sciences

LncRNA PVT1 contributes to invasion and doxorubicin resistance of bladder cancer cells through promoting MDM2 expression and AURKB-mediated p53 ubiquitination

Xiaoqin Jiang et al.

Summary: This study found that lncRNA PVT1 promotes proliferation and drug resistance of bladder cancer cells by upregulating MDM2 expression and AURKB-mediated p53 ubiquitination.

ENVIRONMENTAL TOXICOLOGY (2022)

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Article Immunology

Palmatine attenuates the doxorubicin-induced inflammatory response, oxidative damage and cardiomyocyte apoptosis

Dongliang Cheng et al.

Summary: The study demonstrates that palmatine treatment can alleviate doxorubicin-induced cardiotoxicity, improve cardiac function, and exert protective effects by suppressing inflammatory response, oxidative damage, and cardiomyocyte apoptosis.

INTERNATIONAL IMMUNOPHARMACOLOGY (2022)

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Article Biochemistry & Molecular Biology

Neferine attenuates doxorubicin-induced fibrosis and hypertrophy in H9c2 cells

Bharathi Priya Lohanathan et al.

Summary: This study evaluated the protective effect of neferine on doxorubicin-induced cardiac fibrosis and hypertrophy. The results showed that neferine reduced fibrosis, hypertrophy, and apoptosis in doxorubicin-treated cardiomyoblasts by modulating the expression levels of specific factors.

JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY (2022)

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Article Plant Sciences

Ethanol extracts of Rhaponticum uniflorum (L.) DC flowers attenuate doxorubicin-induced cardiotoxicity via alleviating apoptosis and regulating mitochondrial dynamics in H9c2 cells

Boqin Hu et al.

Summary: This study investigates the cardioprotective effects of ethanol extracts of Loulu flowers (LLF) against doxorubicin-induced cardiotoxicity. The results show that LLF can alleviate DOX-induced cardiotoxicity by regulating mitochondrial dynamics and inhibiting NF-kappa B signaling.

JOURNAL OF ETHNOPHARMACOLOGY (2022)

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Article Oncology

Genome-wide CRISPR screen identified Rad18 as a determinant of doxorubicin sensitivity in osteosarcoma

Mingrui Du et al.

Summary: In this study, Rad18 was identified as a driver of doxorubicin resistance in OS, promoting the activation of the HR pathway. Targeting Rad18 proves to be an effective approach to overcome chemotherapy resistance in OS.

JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH (2022)

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Review Oncology

Targeting autophagy in prostate cancer: preclinical and clinical evidence for therapeutic response

Milad Ashrafizadeh et al.

Summary: This review discusses the role and regulatory mechanisms of autophagy in prostate cancer. Autophagy can impact cancer cell proliferation, survival, and metastasis, as well as the response to therapy. Targeting autophagic genes and utilizing nanotherapeutics show promise in improving patient prognosis.

JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH (2022)

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Article Biotechnology & Applied Microbiology

ADAR2 increases in exercised heart and protects against myocardial infarction and doxorubicin-induced cardiotoxicity

Xiaoting Wu et al.

Summary: Exercise training benefits the heart and upregulates ADAR2 expression in the heart. ADAR2 can regulate the abundance of mature miR-34a in cardiomyocytes and affect their proliferation and apoptosis. This study suggests that ADAR2 overexpression or RNA editing via ADAR2 may be a promising therapeutic strategy for heart diseases.

MOLECULAR THERAPY (2022)

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Article Nutrition & Dietetics

Promising cardioprotective effect of baicalin in doxorubicin-induced cardiotoxicity through targeting toll-like receptor 4/nuclear factor-kB and Wnt/b-catenin pathways

Salwa R. Abo El-Ela et al.

Summary: Baicalin, a flavonoid extracted from Scutellariae baicalensis Georgi, exhibits potential in attenuating doxorubicin-induced cardiotoxicity. It has anti-inflammatory and antioxidant effects, and can inhibit the TLR4/NF-kB pathway while activating the Wnt/β-catenin pathway.

NUTRITION (2022)

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Article Cell Biology

Choline Protects the Heart from Doxorubicin-Induced Cardiotoxicity through Vagal Activation and Nrf2/HO-1 Pathway

Fuding Guo et al.

Summary: This study demonstrates that choline protects the heart from DOX-induced cardiotoxicity by reducing oxidative stress, inflammation, and apoptosis. Choline also modulates the levels of cardiac neurotransmitters and heart rate variability, which contribute to its protective effects.

OXIDATIVE MEDICINE AND CELLULAR LONGEVITY (2022)

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Article Plant Sciences

In vivo and in vitro protective effects of shengmai injection against doxorubicin-induced cardiotoxicity

Peng Zhou et al.

Summary: This study reveals a new mechanism by which Shengmai injection alleviates doxorubicin-induced cardiomyopathy by modulating the Nrf2/Keap1 signaling pathway.

PHARMACEUTICAL BIOLOGY (2022)

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Article Plant Sciences

Total flavonoids of Selaginella tamariscina (P.Beauv.) Spring ameliorates doxorubicin-induced cardiotoxicity by modulating mitochondrial dysfunction and endoplasmic reticulum stress via activating MFN2/PERK

Liyuan Gao et al.

Summary: The present study aimed to investigate the effect of total flavonoids of Selaginella tamariscina (TFST) on doxorubicin-induced cardiotoxicity. The results showed that TFST significantly alleviated doxorubicin-induced mitochondrial dysfunction and endoplasmic reticulum stress. This protective effect was achieved through the activation of the MFN2/PERK pathway.

PHYTOMEDICINE (2022)

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Article Toxicology

Cardioprotective effects of corilagin on doxorubicin induced cardiotoxicity via P13K/Akt and NF-κB signaling pathways in rats model

Jing Huang et al.

Summary: The study demonstrated that corilagin can improve doxorubicin-induced cardiac damage by increasing blood pressure and heart rate levels, and reducing the levels of cardiotoxic enzymes and biomarkers in serum. Histopathological examination showed that corilagin had anti-toxic effects on cardiac tissue, while doxorubicin caused inflammatory cell infiltration, necrosis, and fragmented myofibrils.

TOXICOLOGY MECHANISMS AND METHODS (2022)

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Article Pharmacology & Pharmacy

SIRT4 Suppresses Doxorubicin-Induced Cardiotoxicity by Regulating the AKT/mTOR/Autophagy Pathway

Ling He et al.

Summary: This study found that SIRT4 overexpression could protect against DOX-induced cardiotoxicity by inhibiting Akt/mTOR-dependent autophagy. These findings may provide a potential therapeutic target for DIC.

TOXICOLOGY (2022)

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Article Medical Laboratory Technology

Gasdermin D mediates doxorubicin-induced cardiomyocyte pyroptosis and cardiotoxicity via directly binding to doxorubicin and changes in mitochondrial damage

Bozhi Ye et al.

Summary: This study reveals the crucial role of gasdermin D (GSDMD) in doxorubicin-induced cardiotoxicity. Doxorubicin induces cardiomyocyte pyroptosis in a GSDMD-dependent manner, leading to cardiomyopathy. Deficiency of GSDMD reduces doxorubicin-induced cardiomyopathy. Additionally, GSDMD mediates doxorubicin-induced mitochondrial damage in cardiomyocytes.

TRANSLATIONAL RESEARCH (2022)

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Article Pharmacology & Pharmacy

Oleoylethanolamide as a New Therapeutic Strategy to Alleviate Doxorubicin-Induced Cardiotoxicity

Yeyu Qin et al.

Summary: This study suggests that Oleoylethanolamide (OEA) treatment can protect the heart from the toxic effects of Doxorubicin (DOX). This protective effect is mediated by the activation of TRPV1 channel and upregulation of the PI3K/Akt signaling pathway.

FRONTIERS IN PHARMACOLOGY (2022)

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Article Cell Biology

Higenamine Attenuates Doxorubicin-Induced Cardiac Remodeling and Myocyte Apoptosis by Suppressing AMPK Activation

Cuiliu Jin et al.

Summary: The study showed that HG alleviated chronic myocardial injury induced by DOX by suppressing AMPK activation and ROS production. The research conducted on mice and cardiomyocytes revealed this conclusion, highlighting HG as a potential counteragent to DOX-induced cardiac toxicity.

FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY (2022)

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Article Biochemistry & Molecular Biology

Hydroxytyrosol Prevents Doxorubicin-Induced Oxidative Stress and Apoptosis in Cardiomyocytes

Ivana Sirangelo et al.

Summary: The major phenolic compound HT in olive oil shows potential in counteracting cardiotoxicity induced by Dox while not interfering with its anti-tumor properties. This study identifies HT as a promising molecule for the development of additional therapeutic approaches to prevent anthracycline-related cardiotoxicity and improve antineoplastic treatments.

ANTIOXIDANTS (2022)

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Article Biochemistry & Molecular Biology

Anti-Inflammatory, Anti-Apoptotic, and Antioxidant Roles of Honey, Royal Jelly, and Propolis in Suppressing Nephrotoxicity Induced by Doxorubicin in Male Albino Rats

Hanaa K. Mohamed et al.

Summary: This study evaluated the protective effects of honey, propolis, and royal jelly against nephrotoxicity induced by doxorubicin (DOX). The results demonstrated that combined treatment with honey, royal jelly, and propolis significantly improved the biochemical, histological, and immunohistochemical outcomes associated with DOX-induced nephrotoxicity. qRT-PCR analysis revealed that the combined treatment decreased the expression of the PARP-1 gene and increased the expression levels of the Bcl-2 gene in the DOX group.

ANTIOXIDANTS (2022)

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Article Cardiac & Cardiovascular Systems

MicroRNA-194-5p Attenuates Doxorubicin-Induced Cardiomyocyte Apoptosis and Endoplasmic Reticulum Stress by Targeting P21-Activated Kinase 2

Hongge Fa et al.

Summary: This study reveals that targeting the miR-194-5p/PAK2/XBP1s axis may alleviate DOX-induced cardiotoxicity, providing potential novel targets for the prevention and treatment of cancer patients receiving DOX treatment.

FRONTIERS IN CARDIOVASCULAR MEDICINE (2022)

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Article Biochemistry & Molecular Biology

Extracellular Vesicles Released after Doxorubicin Treatment in Rats Protect Cardiomyocytes from Oxidative Damage and Induce Pro-Inflammatory Gene Expression in Macrophages

Chontida Yarana et al.

Summary: The study indicates that EVs released from DOXO-treated rats have protective effects on cardiomyocytes, reducing ROS production and cell death. However, they have detrimental effects on macrophages, leading to activation of immune responses and suppression. These results highlight the pleiotropic roles of EVs in DIC.

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES (2022)

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Article Biochemistry & Molecular Biology

Adrenomedullin Mitigates Doxorubicin-Induced Nephrotoxicity in Rats: Role of Oxidative Stress, Inflammation, Apoptosis, and Pyroptosis

Rania Nagi Abd-Ellatif et al.

Summary: This study showed that adrenomedullin (ADM) administration could protect against doxorubicin (DOX)-induced nephrotoxicity in rats. The protective effects of ADM may be attributed to its antioxidant, anti-inflammatory, anti-apoptotic, and anti-pyroptotic properties.

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES (2022)

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Article Biochemistry & Molecular Biology

Farnesol Protects against Cardiotoxicity Caused by Doxorubicin-Induced Stress, Inflammation, and Cell Death: An In Vivo Study in Wistar Rats

Abdulrab Ahmed M. Alkhanjaf et al.

Summary: The study demonstrates that farnesol can reduce cardiac injuries caused by doxorubicin through its antioxidant, anti-inflammatory, and anti-apoptotic potential.

MOLECULES (2022)

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Article Biochemistry & Molecular Biology

Protective Effects of Hippophae rhamnoides L. Phenylpropanoids on Doxorubicin-Induced Cardiotoxicity in Zebrafish

Gang Li et al.

Summary: This study found that phenylpropanoid compounds extracted from sea buckthorn can significantly alleviate Doxorubicin-induced cardiac injury in zebrafish by stabilizing mitochondrial biogenesis and function.

MOLECULES (2022)

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Article Biochemistry & Molecular Biology

Gemigliptin exerts protective effects against doxorubicin-induced hepatotoxicity by inhibiting apoptosis via the regulation of fibroblast growth factor 21 expression

Kyeong-Min Lee et al.

Summary: This study investigates the protective effects of gemigliptin on doxorubicin-induced hepatotoxicity by upregulating fibroblast growth factor 21 expression.

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS (2022)

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Article Multidisciplinary Sciences

A RGS7-CaMKII complex drives myocyte-intrinsic and myocyte- extrinsic mechanisms of chemotherapy-induced cardiotoxicity

Madhuri Basak et al.

Summary: This study identifies RGS7 as a key driver of chemotherapy-induced oxidative stress, cell loss, and fibrosis in the heart. Importantly, RGS7 does not impact the sensitivity of cancer cells to chemotherapeutic drugs. Therefore, RGS7 emerges as a potential therapeutic target for detecting or mitigating chemotherapy-associated cardiac damage.

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA (2022)

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Article Biochemistry & Molecular Biology

Exploring the role of ferroptosis in the doxorubicin-induced chronic cardiotoxicity using a murine model

Xiaofen Li et al.

Summary: The study established a murine model of DOX-induced chronic cardiotoxicity, showing significant changes in heart function and structure with increased cumulative DOX dose, as well as iron overload in heart tissue. Ferroptosis may be induced by inhibiting Slc7a11 in system-Xc.

CHEMICO-BIOLOGICAL INTERACTIONS (2022)

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Article Biochemical Research Methods

Solid Lipid Nanoformulation of Berberine Attenuates Doxorubicin Triggered in vitro Inflammation in H9c2 Rat Cardiomyocytes

Shalini Rawal et al.

Summary: This study aimed to evaluate the efficacy of solid lipid nanoparticles (SLNs) of berberine against doxorubicin-induced cardiotoxicity. The results showed that Ber-SLNs effectively prevented inflammation and oxidative stress caused by doxorubicin in rat cardiomyocytes.

COMBINATORIAL CHEMISTRY & HIGH THROUGHPUT SCREENING (2022)

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Review Nutrition & Dietetics

Effects of Ginger Intake on Chemotherapy-Induced Nausea and Vomiting: A Systematic Review of Randomized Clinical Trials

Jihee Choi et al.

Summary: The study aimed to evaluate the effect of ginger supplementation as an adjuvant treatment for alleviating chemotherapy-induced nausea and vomiting. The results showed that ginger supplementation may reduce the incidence of acute chemotherapy-induced vomiting.

NUTRIENTS (2022)

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Review Pharmacology & Pharmacy

SIRT1 activation and its effect on intercalated disc proteins as a way to reduce doxorubicin cardiotoxicity

Ekaterina Podyacheva et al.

Summary: Neoplasm is a major cause of morbidity and mortality worldwide. The use of cytotoxic drugs, such as doxorubicin, in cancer treatment is associated with cardiovascular complications. Defects in intercalated disc proteins can lead to cardiovascular diseases, including doxorubicin-induced cardiomyopathy. Activation of SIRT1 may provide cardioprotection by improving cellular and mitochondrial functions, reducing oxidative stress, and protecting intercalated disc structures.

FRONTIERS IN PHARMACOLOGY (2022)

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Article Medicine, Research & Experimental

Infliximab and/or MESNA alleviate doxorubicin-induced Alzheimer's disease-like pathology in rats: A new insight into TNF-α/Wnt/β-catenin signaling pathway

Hoda E. Mohamad et al.

Summary: The current study aimed to investigate the neurotoxic potential of DOX in inducing AD-like pathology and the efficacy of infliximab (IFX) and 2-mercaptoethane sulfonate sodium (MESNA) in attenuating DOX-induced neurotoxicity. The results showed that both IFX and MESNA significantly mitigated DOX-induced brain injury, neuroinflammation, and apoptosis, with the best improvement observed with their combined administration.

LIFE SCIENCES (2022)

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Article Biochemistry & Molecular Biology

Maleimide-Functionalized Liposomes: Prolonged Retention and Enhanced Efficacy of Doxorubicin in Breast Cancer with Low Systemic Toxicity

Chuane Tang et al.

Summary: The surface modification of liposomes with maleimide group prolongs the retention time of anticancer drug doxorubicin at tumor sites and enhances its efficacy. The modified liposomes exhibit stronger inhibitory effect against tumor cells and lower cardiotoxicity in mice bearing tumor xenografts.

MOLECULES (2022)

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Article Plant Sciences

Isoorientin attenuates doxorubicin-induced cardiac injury via the activation of MAPK, Akt, and Caspase-dependent signaling pathways

Shaoguang Li et al.

Summary: The combination of isoorientin (ISO) and doxorubicin (DOX) synergistically enhances the anti-proliferative effect of DOX on various tumor cells and improves the survival rate of DOX-injured cardiomyocytes by reducing reactive oxygen species, maintaining mitochondrial function, and inhibiting apoptosis. ISO also exhibits a dose-dependent protective effect on DOX-induced heart injury in mice, possibly through the inhibition of MAPK and caspase-dependent apoptosis pathways.

PHYTOMEDICINE (2022)

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Article Plant Sciences

Spinacetin alleviates doxorubicin-induced cardiotoxicity by initiating protective autophagy through SIRT3/AMPK/mTOR pathways

Dawei Liu et al.

Summary: This study aimed to investigate the effects of spinacetin on doxorubicin-induced cardiotoxicity and found that spinacetin can protect cardiomyocytes from damage by activating autophagy pathways.

PHYTOMEDICINE (2022)

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Article Pharmacology & Pharmacy

Ononin alleviates endoplasmic reticulum stress in doxorubicin-induced cardiotoxicity by activating SIRT3

Hanlin Zhang et al.

Summary: Ononin has cardioprotective effects by ameliorating DOX-induced myocardial injury and restoring cardiac dysfunction. It can also suppress DOX-induced ER stress and apoptosis, possibly mediated by stimulation of the SIRT3 pathway.

TOXICOLOGY AND APPLIED PHARMACOLOGY (2022)

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Article Toxicology

Scutellarin attenuates doxorubicin-induced oxidative stress, DNA damage, mitochondrial dysfunction, apoptosis and autophagy in H9c2 cells, cardiac fibroblasts and HUVECs

Li Zhou et al.

Summary: This study investigated the toxicity of doxorubicin (DOX) on cardiomyocytes, cardiac fibroblasts, and endothelial cells. It was found that DOX had a greater killing effect on cardiomyocytes compared to the other cell types. Additionally, the protective effects of scutellarin (SCU) on DOX-induced cytotoxicity were explored, showing that SCU attenuated oxidative stress, DNA damage, mitochondrial dysfunction, apoptosis, and autophagy induced by DOX.

TOXICOLOGY IN VITRO (2022)

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Article Cell Biology

Exogenous 8-hydroxydeoxyguanosine attenuates doxorubicin-induced cardiotoxicity by decreasing pyroptosis in H9c2 cardiomyocytes

Soyoung Hwang et al.

Summary: Doxorubicin can induce cardiomyopathy through pyroptosis involving NLRP3 inflammasome and GSDMD. Treatment with 8-OHdG has shown to reduce DOX-induced pyroptosis, suggesting it may attenuate cardiotoxic effects of DOX.

BMC MOLECULAR AND CELL BIOLOGY (2022)

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Article Pharmacology & Pharmacy

Cariporide Attenuates Doxorubicin-Induced Cardiotoxicity in Rats by Inhibiting Oxidative Stress, Inflammation and Apoptosis Partly Through Regulation of Akt/GSK-3β and Sirt1 Signaling Pathway

Wenli Liao et al.

Summary: The study demonstrated that CAR has significant protective effects against DOX-induced cardiotoxicity in rats by suppressing oxidative stress, inflammation, and apoptosis, at least in part, through regulation of Akt/GSK-3 beta and Sirt1 signaling pathway.

FRONTIERS IN PHARMACOLOGY (2022)

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Article Pharmacology & Pharmacy

Combination of Panax ginseng C. A. Mey and Febuxostat Boasted Cardioprotective Effects Against Doxorubicin-Induced Acute Cardiotoxicity in Rats

Hayder M. Al-Kuraishy et al.

Summary: The present study assessed the cardioprotective effects of P. ginseng and febuxostat, and their combination, against DOX-induced cardiotoxicity. The combination of P. ginseng and febuxostat showed significant improvement in biomarkers of acute DOX-induced cardiotoxicity. The potential mechanism of this combination was mainly mediated by the anti-inflammatory and antioxidant effects of P. ginseng and febuxostat.

FRONTIERS IN PHARMACOLOGY (2022)

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Article Medicine, General & Internal

Upregulation of Endothelin-1 May Predict Chemotherapy-Induced Cardiotoxicity in Women with Breast Cancer

Krithika Krishnarao et al.

Summary: As survival rates increase in breast cancer patients due to newer therapies, concerns about chemotherapy-induced cardiotoxicity have emerged. This study examined ATR1 and ET1 expression in breast cancer tissue and found that increased ET1 expression is associated with reduced LVEF, suggesting it may serve as a tissue biomarker for predicting the risk of developing chemotherapy-induced cardiotoxicity in women with breast cancer.

JOURNAL OF CLINICAL MEDICINE (2022)

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Review Cell Biology

Mitochondria and Doxorubicin-Induced Cardiomyopathy: A Complex Interplay

Leonardo Schirone et al.

Summary: Cardiotoxicity is a major side effect of doxorubicin treatment, affecting nearly 30% of patients within 5 years after chemotherapy. Despite identifying various molecular mechanisms explaining the cardiac derangements induced by doxorubicin, the translation to clinical practice remains challenging. This review focuses on mitochondria and discusses the pathophysiology, epidemiology, and detrimental effects of doxorubicin on mitochondrial function.

CELLS (2022)

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Review Oncology

Emerging role of non-coding RNAs in glucose metabolic reprogramming and chemoresistance in colorectal cancer

Shushan Yan et al.

Summary: Metabolic reprogramming, especially glucose metabolic reprogramming, plays a crucial role in colorectal cancer by shaping cellular phenotypes and promoting uncontrolled proliferation. Non-coding RNAs have been implicated in glucose metabolic reprogramming and chemoresistance, suggesting their potential as key regulators in CRC pathogenesis. Understanding the interplay between ncRNAs and glucose metabolic reprogramming may lead to the discovery of novel biomarkers for the diagnosis and prognosis prediction of CRC.

FRONTIERS IN ONCOLOGY (2022)

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Article Immunology

Doxorubicin-Induced Cardiotoxicity May Be Alleviated by Bone Marrow Mesenchymal Stem Cell-Derived Exosomal lncRNA via Inhibiting Inflammation

Chao Tian et al.

Summary: In this study, it was found through high-throughput sequencing and transcriptome bioinformatics analysis that the lncRNA MSTRG.58791.2 derived from BMSC-Exos can alleviate DOX-induced cardiotoxicity by suppressing inflammatory response and inflammation-related cell death.

JOURNAL OF INFLAMMATION RESEARCH (2022)

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Article Integrative & Complementary Medicine

Activation of p62-NRF2 Axis Protects against Doxorubicin-Induced Ferroptosis in Cardiomyocytes: A Novel Role and Molecular Mechanism of Resveratrol

Wei Yu et al.

Summary: Doxorubicin, a common chemotherapeutic agent, has limited clinical efficacy due to its severe cardiotoxicity. Resveratrol, known for its antioxidative and anti-inflammatory properties, protects cardiomyocytes by inhibiting ferroptosis induced by doxorubicin. This study reveals that resveratrol activates the p62-NRF2/HO-1 pathway and suppresses mitochondrial reactive oxygen species, thereby preventing ferroptosis in cardiomyocytes.

AMERICAN JOURNAL OF CHINESE MEDICINE (2022)

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Article Biochemistry & Molecular Biology

Baicalin regulates TLR4/IkBa/NFkB signaling pathway to alleviate inflammation in Doxorubicin related cardiotoxicity

Panpan Feng et al.

Summary: This article investigates the cardiotoxicity of doxorubicin and the protective effect of baicalein, focusing on the role of the TLR4/IκBα/NF-κB signaling pathway and inflammatory markers.

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS (2022)

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Article Pharmacology & Pharmacy

The effect and mechanistic study of encequidar on reversing the resistance of SW620/AD300 cells to doxorubicin

Hang Zhang et al.

Summary: Encequidar, a gut-specific P-glycoprotein (P-gp) inhibitor, has been shown to reverse drug resistance in metastatic breast cancer. In this study, encequidar was synthesized and its pharmacological effect on drug-resistant colon cancer cells was investigated. The results revealed that encequidar reduced drug efflux, enhanced cytotoxicity, and promoted tumor apoptosis. Metabolomic analysis showed that encequidar and the drug doxorubicin affected the citric acid cycle, glutathione metabolism, and reactive oxygen species production, leading to increased sensitivity of drug-resistant cells to doxorubicin.

BIOCHEMICAL PHARMACOLOGY (2022)

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Article Biochemistry & Molecular Biology

Cardiolipin nanodisks confer protection against doxorubicin-induced mitochondrial dysfunction

Colin A. Fox et al.

Summary: Doxorubicin (DOX) is a widely used aqueous soluble anthracycline therapeutic in cancer treatment, with its anti-cancer activity being dose-dependent and the risk of cardiotoxicity increasing with higher dosage. DOX binds to cardiolipin (CL) and association with CL-nanodisks (CL-ND) does not diminish its cancer cell growth inhibition activity while protecting cardiomyocytes from DOX-induced effects.

BIOCHIMICA ET BIOPHYSICA ACTA-BIOMEMBRANES (2022)

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Article Medicine, Research & Experimental

Potential cardioprotective effects of Amentoflavone in doxorubicin-induced cardiotoxicity in mice

Fatemah A. Alherz et al.

Summary: Amentoflavone (AMF) has cardioprotective effects against doxorubicin (DOX) cardiotoxicity through its antioxidant, anti-inflammatory, anti-apoptotic effects and restoration of mitochondrial function.

BIOMEDICINE & PHARMACOTHERAPY (2022)

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Article Medicine, Research & Experimental

Puerarin activates adaptive autophagy and protects the myocardium against doxorubicin-induced cardiotoxicity via the 14-3-3γ/PKCε pathway

Yian Peng et al.

Summary: The study found that Pue pretreatment can protect the myocardium against doxorubicin-induced cardiotoxicity by activating adaptive autophagy through the 14-3-3 gamma/PKC epsilon pathway.

BIOMEDICINE & PHARMACOTHERAPY (2022)

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Article Cardiac & Cardiovascular Systems

Proteasomal Degradation of TRAF2 Mediates Mitochondrial Dysfunction in Doxorubicin-Cardiomyopathy

Rimpy Dhingra et al.

Summary: The study reveals that doxorubicin (DOX) interferes with NF-κB activation by TNFα in cardiac myocytes, possibly due to proteasomal degradation of TRAF2. The degradation of TRAF2 is regulated by cellular inhibitors of apoptosis 1 and USP19. Loss of TRAF2 leads to increased sensitivity of cardiac myocytes to TNFα-mediated necrotic cell death and DOX cardiotoxicity.

CIRCULATION (2022)

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Article Biochemistry & Molecular Biology

Exosomal thioredoxin-1 from hypoxic human umbilical cord mesenchymal stem cells inhibits ferroptosis in doxorubicin-induced cardiotoxicity via mTORC1 signaling

Yue Yu et al.

Summary: This study compared the therapeutic effects of normoxic and hypoxic human umbilical cord mesenchymal stem cell-derived exosomes (Exo and Hypo-Exo) on doxorubicin (DOX)-induced ferroptosis and explored the underlying mechanisms. The results showed that Hypo-Exo exhibited better suppression of DOX-induced ferroptosis by regulating the Trx1-mTORC1-GPX4 pathway. This study suggests that Hypo-Exo may be a potential strategy against ferroptosis in DOX-induced cardiotoxicity.

FREE RADICAL BIOLOGY AND MEDICINE (2022)

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Article Biochemistry & Molecular Biology

Disruption of histamine/H1R-STAT3-SLC7A11 axis exacerbates doxorubicin-induced cardiac ferroptosis

Xiaowei Zhu et al.

Summary: This study reveals the role of the histamine/H1R signaling pathway in doxorubicin-induced cardiotoxicity. Histamine deficiency or H1R antagonism accelerates myocardial ferroptosis and aggravates doxorubicin-induced cardiotoxicity. These findings provide a potential target for the treatment of doxorubicin-induced cardiotoxicity.

FREE RADICAL BIOLOGY AND MEDICINE (2022)

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Article Biochemistry & Molecular Biology

Dapagliflozin Mitigates Doxorubicin-Caused Myocardium Damage by Regulating AKT-Mediated Oxidative Stress, Cardiac Remodeling, and Inflammation

Pei-Ling Hsieh et al.

Summary: This study demonstrated that dapagliflozin could mitigate doxorubicin-induced cardiotoxicity by reducing oxidative stress, improving mitochondrial dysfunction, decreasing fibrosis, hypertrophy, and inflammation through the PI3K/AKT/Nrf2 signaling pathway.

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES (2022)

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Article Biochemistry & Molecular Biology

Fucoidan Protects against Doxorubicin-Induced Cardiotoxicity by Reducing Oxidative Stress and Preventing Mitochondrial Function Injury

Yuting Ji et al.

Summary: Fucoidan has potent protective effects against DOXO-induced cardiotoxicity by reducing oxidative stress and preventing mitochondrial function injury.

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES (2022)

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Article Cell Biology

CaMKII orchestrates endoplasmic reticulum stress and apoptosis in doxorubicin-induced cardiotoxicity by regulating the IRE1α/XBP1s pathway

Lingheng Kong et al.

Summary: This study found that CaMKII exacerbates Dox-induced cardiotoxicity by regulating the IRE1α/XBP1s pathway. Inhibition of CaMKII can improve cardiac dysfunction and pathological myocardial changes induced by Dox, preventing endoplasmic reticulum stress and apoptosis.

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE (2022)

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Article Plant Sciences

Cinobufagin inhibits tumor progression and reduces doxorubicin resistance by enhancing FOXO1-mediated transcription of FCGBP in osteosarcoma

Xiucai Ma et al.

Summary: Cinobufagin, an active ingredient in traditional Chinese medicine, can treat bone pathological conditions. This study explored the roles and mechanisms of cinobufagin in osteosarcoma development and doxorubicin resistance. The results showed that cinobufagin suppressed tumor progression and reduced resistance to doxorubicin through potentiation of FOXO1-mediated transcription of FCGBP.

JOURNAL OF ETHNOPHARMACOLOGY (2022)

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Article Oncology

Hsa_circ_0000098 is a novel therapeutic target that promotes hepatocellular carcinoma development and resistance to doxorubicin

Yi Li et al.

Summary: This study discovered that circ_0000098 is an oncogenic circRNA that promotes the development of HCC through the miR-383/MCUR1 axis. Currently, targeting circ_0000098 with DOX/sh-1@PLT holds promising and practical therapeutic potential for preventing DOX resistance in HCC.

JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH (2022)

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Article Oncology

CircRNA-CREIT inhibits stress granule assembly and overcomes doxorubicin resistance in TNBC by destabilizing PKR

Xiaolong Wang et al.

Summary: Our study revealed the downregulation of circRNA-CREIT in doxorubicin resistant TNBC cells and its association with poor prognosis. We identified the RNA binding protein DHX9 as responsible for the reduction in circRNA-CREIT by interacting with the flanking inverted repeat Alu (IRAlu) sequences and inhibiting back-splicing. Mechanistically, circRNA-CREIT acted as a scaffold to facilitate the interaction between PKR and the E3 ligase HACE1, leading to proteasomal degradation of PKR protein via K48-linked polyubiquitylation and attenuation of the assembly of stress granules (SGs) to activate the RACK1/MTK1 apoptosis signaling pathway. Moreover, circRNA-CREIT could be packaged into exosomes and disseminate doxorubicin sensitivity among TNBC cells.

JOURNAL OF HEMATOLOGY & ONCOLOGY (2022)

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Review Pharmacology & Pharmacy

Doxorubicin-induced cardiotoxicity: causative factors and possible interventions

Isobel C. Jones et al.

Summary: Doxorubicin is widely used as a chemotherapeutic agent, but its cardiotoxicity limits its application. The understanding of Doxorubicin metabolism and mechanisms of action is still incomplete, and the mechanisms of Doxorubicin-induced cardiotoxicity are multifactorial and involve oxidative stress. Novel delivery systems and antioxidant therapies are important for reducing cardiotoxicity.

JOURNAL OF PHARMACY AND PHARMACOLOGY (2022)

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Article Medicine, Research & Experimental

Protective effect of green synthesized Selenium Nanoparticles against Doxorubicin induced multiple adverse effects in Swiss albino mice

Mohammad Afsar Khan et al.

Summary: The biosynthesized SeNP conjugated with DOX showed a protective effect against DOX-induced toxicities by reducing reactive oxygen and nitrogen species, DNA damage, and lipid peroxidation, and restoring antioxidant defense systems and cytoarchitectures.

LIFE SCIENCES (2022)

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Review Cell Biology

Mechanisms and Drug Intervention for Doxorubicin-Induced Cardiotoxicity Based on Mitochondrial Bioenergetics

Guanjing Ling et al.

Summary: This article summarizes the related mechanisms of Doxorubicin-induced cardiac mitochondrial bioenergetics disorders, including mitochondrial substrate metabolism, the mitochondrial respiratory chain, myocardial ATP storage and utilization, and other mechanisms affecting mitochondrial bioenergetics. It also summarizes the interventions for these disorders using chemical drugs and traditional herbal medicine, providing a comprehensive process for studying and developing therapeutic strategies for DIC.

OXIDATIVE MEDICINE AND CELLULAR LONGEVITY (2022)

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Article Plant Sciences

Tanshinone I inhibits doxorubicin-induced cardiotoxicity by regulating Nrf2 signaling pathway

Qianqian Jiang et al.

Summary: This study demonstrated that Tanshinone I (Tan I) can protect against Doxorubicin-induced cardiotoxicity (DIC) by reducing oxidative stress and maintaining mitochondrial function. This protective effect is mediated by the activation of the nuclear erythroid factor 2-related factor 2 (Nrf2) pathway.

PHYTOMEDICINE (2022)

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Article Plant Sciences

Natural compound glycyrrhetinic acid protects against doxorubicin-induced cardiotoxicity by activating the Nrf2/HO-1 signaling pathway

Yanfen Cheng et al.

Summary: Glycyrrhetinic acid (GA) protects against doxorubicin-induced cardiotoxicity by suppressing oxidative stress, mitochondrial dysfunction, and apoptosis via upregulating the Nrf2/HO-1 signaling pathway.

PHYTOMEDICINE (2022)

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Article Biochemistry & Molecular Biology

Doxorubicin causes ferroptosis and cardiotoxicity by intercalating into mitochondrial DNA and disrupting Alas1-dependent heme synthesis

Ko Abe et al.

Summary: The clinical use of doxorubicin is limited due to its cardiotoxicity. This study found that doxorubicin accumulates in mitochondria and induces iron-dependent cell death called ferroptosis in cardiomyocytes. Disruption of heme synthesis and impaired iron utilization contribute to this process. Additionally, administration of 5-aminolevulinic acid can prevent doxorubicin-induced cardiotoxicity.

SCIENCE SIGNALING (2022)

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Article Pharmacology & Pharmacy

Sphingosylphosphorylcholine ameliorates doxorubicin-induced cardiotoxicity in zebrafish and H9c2 cells by reducing excessive mitophagy and mitochondrial dysfunction

Jinrun Zhou et al.

Summary: This study found that targeting sphingosylphosphorylcholine (SPC) can alleviate doxorubicin (DOX)-induced cardiotoxic damage. SPC can restore mitochondrial homeostasis, reduce cell apoptosis, and ameliorate myocardial injury caused by DOX. This suggests that reducing the cardiotoxicity of chemotherapeutic drugs by targeting SPC may be a new solution.

TOXICOLOGY AND APPLIED PHARMACOLOGY (2022)

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Article Cell Biology

Gasdermin D mediates endoplasmic reticulum stress via FAM134B to regulate cardiomyocyte autophagy and apoptosis in doxorubicin-induced cardiotoxicity

Ya'nan Qu et al.

Summary: GSDMD regulates the interaction between FAM134B and LC3, promoting autophagy and inducing cardiomyocyte apoptosis, thus exacerbating doxorubicin-induced cardiotoxicity.

CELL DEATH & DISEASE (2022)

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Article Medicine, Research & Experimental

Thymoquinone-induced autophagy mitigates doxorubicin-induced H9c2 cell apoptosis

Dawei Liu et al.

Summary: Our study found that pretreatment with TQ can reduce Dox-induced cardiomyocyte death and apoptosis. TQ also upregulates autophagy through activation of the LKB1/AMPK pathways, further enhancing the protective effect against Dox toxicity in cardiomyocytes.

EXPERIMENTAL AND THERAPEUTIC MEDICINE (2022)

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Article Nutrition & Dietetics

Resveratrol and FGF1 Synergistically Ameliorates Doxorubicin-Induced Cardiotoxicity via Activation of SIRT1-NRF2 Pathway

Guangping Lu et al.

Summary: This study aimed to explore the therapeutic potential and underlying mechanisms of the co-treatment of resveratrol (RES) and fibroblast growth factor 1 (FGF1) in a doxorubicin (DOX)-treated model. The results showed that RES could reduce the growth-promoting activity of FGF1 and exhibited a more powerful antioxidative capacity in a DOX-treated model, with cardioprotective action mediated through the SIRT1/NRF2 pathway.

NUTRIENTS (2022)

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Article Pharmacology & Pharmacy

Danhong injection attenuates doxorubicin-induced cardiotoxicity in rats via suppression of apoptosis: network pharmacology analysis and experimental validation

Xiaojiao Yi et al.

Summary: The present study aimed to evaluate the potential protective effect of Danhong injection (DHI) on doxorubicin (DOX)-induced cardiotoxicity and investigate the underlying mechanisms. Results showed that DHI treatment attenuated the cardiotoxicity induced by DOX, possibly through regulating the apoptosis pathway.

FRONTIERS IN PHARMACOLOGY (2022)

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Review Medicine, Research & Experimental

Research progress of therapeutic drugs for doxorubicin-induced cardiomyopathy

Ye Chen et al.

Summary: Doxorubicin (DOX) is an effective chemotherapy agent for treating malignant tumors, but its use is limited due to dose-dependent cardiotoxicity. This study evaluates the effects of various drugs on DOX-induced cardiomyopathy, providing insights for future clinical treatment.

BIOMEDICINE & PHARMACOTHERAPY (2022)

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Article Cardiac & Cardiovascular Systems

Calsyntenin-1 Promotes Doxorubicin-induced Dilated Cardiomyopathy in Rats

Mingxiang Zhu et al.

Summary: Our findings demonstrated that CLSTN1 promotes the pathogenesis of doxorubicin-induced DCM. CLSTN1 could be a therapeutic target to prevent the development of doxorubicin-induced DCM.

CARDIOVASCULAR DRUGS AND THERAPY (2022)

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Article Biochemistry & Molecular Biology

The SPATA2/CYLD pathway contributes to doxorubicin-induced cardiomyocyte ferroptosis via enhancing ferritinophagy

Yuan-Jing Zhou et al.

Summary: This study identifies a novel pathway, SPATA2/CYLD, which contributes to doxorubicin-induced cardiomyocyte ferroptosis by enhancing ferritinophagy through deubiquitination of NCOA4. Knockdown of SPATA2 attenuates cardiomyocyte injury and ferroptosis.

CHEMICO-BIOLOGICAL INTERACTIONS (2022)

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Article Cell Biology

Nootkatone Ameliorates Doxorubicin Induced Myocardial Injury through Modulation of NF-κB Signals and Oxidative Stress

Suhail Al-Salam et al.

Summary: Doxorubicin is a potent chemotherapeutic drug, but its usage is limited due to serious side effects, especially cardiotoxicity. Nootkatone has been found to improve Doxorubicin-induced myocardial injury through modulation of NF-kappa B signals and reduction of oxidative stress.

CELLULAR PHYSIOLOGY AND BIOCHEMISTRY (2022)

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Article Toxicology

Phosphodiesterase inhibitor, Vinpocetine, guards against doxorubicin induced cardiotoxicity via modulation of HIF/VEGF and cGMP/cAMP/SIRT signaling pathways

Marwa M. M. Refaie et al.

Summary: The study found that vinpocetine can protect the heart from doxorubicin-induced damage through various mechanisms, including modulating signaling pathways, enhancing antioxidant capacity, and reducing inflammation levels.

HUMAN & EXPERIMENTAL TOXICOLOGY (2022)

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Article Biochemistry & Molecular Biology

CIRBP-OGFR axis safeguards against cardiomyocyte apoptosis and cardiotoxicity induced by chemotherapy

Cihang Liu et al.

Summary: CIRBP plays an important role in chemotherapy-induced cardiotoxicity by reducing cardiomyocyte apoptosis and attenuating cardiac toxicity through disrupting the OGF-OGFR signal. CIRBP interacts with OGFR mRNA and represses OGFR expression by reducing mRNA stability.

INTERNATIONAL JOURNAL OF BIOLOGICAL SCIENCES (2022)

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Article Engineering, Biomedical

M2-like macrophages transplantation protects against the doxorubicin-induced heart failure via mitochondrial transfer

Yihai Liu et al.

Summary: The adoptive transfer of M2-like macrophages induced by M-CSF and IL-4 can improve doxorubicin-induced cardiotoxicity in heart failure, reduce cardiac fibrosis and cardiomyocyte apoptosis, increase circulating IL-4 levels, and provide protection through mitochondrial transfer.

BIOMATERIALS RESEARCH (2022)

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Article Engineering, Environmental

Tumor-specific carrier-free nanodrugs with GSH depletion and enhanced ROS generation for endogenous synergistic anti-tumor by a chemotherapy-photodynamic therapy

Jin-Shuai Lan et al.

Summary: Combining chemotherapy and photodynamic therapy with a novel carrier-free nanodrug has shown promising results in enhancing treatment efficacy, indicating that depleting GSH through chemotherapy can improve the effectiveness of PDT.

CHEMICAL ENGINEERING JOURNAL (2021)

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Article Oncology

Ginger Extract Loaded into Chitosan Nanoparticles Enhances Cytotoxicity and Reduces Cardiotoxicity of Doxorubicin in Hepatocellular Carcinoma in Mice

Hend E. Abo Mansour et al.

Summary: This study found that CNPs loaded with GE and DXN significantly enhanced cytotoxicity and reduced cardiotoxicity induced by DOX. In a mouse model, GE CNPs showed higher anticancer activity against HepG2 cells and improved liver tissue structure and cardiac indicators, indicating the potential for treating HCC.

NUTRITION AND CANCER-AN INTERNATIONAL JOURNAL (2021)

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Article Pharmacology & Pharmacy

Cardioprotective effects of melatonin and metformin against doxorubicin-induced cardiotoxicity in rats are through preserving mitochondrial function and dynamics

Apiwan Arinno et al.

Summary: Studies have shown that melatonin and metformin can reduce oxidative stress, inflammation, autophagy, apoptosis, and improve mitochondrial function to protect against Doxorubicin-induced cardiotoxicity.

BIOCHEMICAL PHARMACOLOGY (2021)

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Article Biochemistry & Molecular Biology

Proanthocyanidin alleviates doxorubicin-induced cardiac injury by inhibiting NF-kB pathway and modulating oxidative stress, cell cycle, and fibrogenesis

Kadry M. Sadek et al.

Summary: This study demonstrates the preventive effect of proanthocyanidin extract against doxorubicin-induced cardiotoxicity in rats by modulating multiple signaling pathways and cytokine expression pathways to alleviate cardiac damage.

JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY (2021)

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Article Oncology

Shengxian decoction decreases doxorubicin-induced cardiac apoptosis by regulating the TREM1/NF-κB signaling pathway

Lei Yao et al.

Summary: Shengxian Decoction (SXT) is a traditional Chinese medicine with cardioprotective effects against doxorubicin (DOX)-induced cardiomyocyte injuries. It was found that SXT inhibits apoptosis and NF-kappa B activation induced by DOX through downregulation of Triggering Receptors Expressed on Myeloid Cells 1 (TREM1). Additionally, SXT significantly reversed DOX-induced cardiotoxicity in rats.

MOLECULAR MEDICINE REPORTS (2021)

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Article Chemistry, Medicinal

Roflumilast Attenuates Doxorubicin-Induced Cardiotoxicity by Targeting Inflammation and Cellular Senescence in Cardiomyocytes Mediated by SIRT1

Sheng Zhang et al.

Summary: The study demonstrates that Roflumilast may alleviate Doxorubicin-induced inflammation and cellular senescence in cardiomyocytes by upregulating SIRT1. This finding provides a new therapeutic approach for managing the cardiotoxicity of Doxorubicin.

DRUG DESIGN DEVELOPMENT AND THERAPY (2021)

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Article Biochemistry & Molecular Biology

An in vivo and in vitro model on the protective effect of corilagin on doxorubicin-induced cardiotoxicity via regulation of apoptosis and PI3-K/AKT signaling pathways

Lianqin Ding et al.

Summary: The study evaluated the action of corilagin on doxorubicin-induced cardiotoxicity and found that it can alleviate doxorubicin-induced cardiac damage by modulating cardio apoptosis and oxidative stress.

JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY (2021)

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Article Medicine, Research & Experimental

Novel in vivo potential of trifluoperazine to ameliorate doxorubicin-induced cardiotoxicity involves suppression of NF-ΚB and apoptosis

Ahmed E. Goda et al.

Summary: Trifluoperazine demonstrates protective effects against doxorubicin-induced cardiotoxicity by alleviating heart failure, inflammation, and myofibril degeneration. Furthermore, trifluoperazine improves renal and hepatic impairments caused by doxorubicin, suggesting its potential in ameliorating organ toxicity.

LIFE SCIENCES (2021)

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Article Biotechnology & Applied Microbiology

Doxorubicin nanomedicine based on ginsenoside Rg1 with alleviated cardiotoxicity and enhanced antitumor activity

Chaoqi Li et al.

Summary: Encapsulating Doxorubicin in nanoparticles containing ginseng component could enhance its anticancer effects and decrease harm to the heart. The Dox@Rg1 nanoparticles demonstrated excellent tumor-targeting ability and improved antitumor effects in vivo.

NANOMEDICINE (2021)

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Article Plant Sciences

Ginsenoside Rb1 ameliorates cardiotoxicity triggered by aconitine via inhibiting calcium overload and pyroptosis

Min Wang et al.

Summary: This study demonstrated that Ginsenoside Rb1 can alleviate aconitine-induced cardiotoxicity by regulating calcium channels, reducing calcium levels, restoring calcium homeostasis, and inhibiting apoptosis and pyroptosis in both rat and human induced pluripotent stem cell-derived cardiomyocytes.

PHYTOMEDICINE (2021)

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Article Chemistry, Applied

Green synthesis of NiONPs using Trigonella subenervis extract and its applications as a highly efficient electrochemical sensor, catalyst, and antibacterial agent

Behnam Mahdavi et al.

Summary: This study demonstrated the green synthesis of NiONPs using Trigonella subenervis extract and characterized the nanoparticles for their potential applications in catalysis, electrochemical sensing, and antibacterial activity. The biosynthesized NiONPs showed uniform spherical morphology with promising results in various assays, highlighting their versatile properties and wide range of potential applications.

APPLIED ORGANOMETALLIC CHEMISTRY (2021)

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Article Medicine, Research & Experimental

Calycosin attenuates doxorubicin-induced cardiotoxicity via autophagy regulation in zebrafish models

Xiaoguang Lu et al.

Summary: Anthracyclines are effective chemotherapeutics for cancer treatment, but they can lead to cardiotoxicity. Calycosin (CA) extracted from traditional Chinese medicine Astragalus may reverse chronic anthracycline-induced cardiotoxicity by modulating autophagy. Further research is needed to understand the mechanism of CA regulation of autophagy.

BIOMEDICINE & PHARMACOTHERAPY (2021)

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Article Biochemistry & Molecular Biology

Irisin ameliorates doxorubicin-induced cardiac perivascular fibrosis through inhibiting endothelial-to-mesenchymal transition by regulating ROS accumulation and autophagy disorder in endothelial cells

Jian-An Pan et al.

Summary: The study revealed the protective role of irisin in EndMT and perivascular fibrosis in the cardiac microenvironment in a mouse DIC model, potentially reversing ROS accumulation and autophagy disorders by regulating UCP2. Irisin was found to be mainly secreted by cardiomyocytes and had a paracrine protective effect on endothelial cells. This study provides a novel perspective on the pathogenesis and potential treatment of DIC.

REDOX BIOLOGY (2021)

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Article Biochemistry & Molecular Biology

Epigallocatechin-3-gallate pretreatment alleviates doxorubicin-induced ferroptosis and cardiotoxicity by upregulating AMPKα2 and activating adaptive autophagy

Huan He et al.

Summary: The mechanism of Doxorubicin-induced cardiotoxicity is complex, involving multiple cell death forms, with clinical intervention effect not ideal. By inhibiting iron accumulation, oxidative stress, and abnormal lipid metabolism, it is possible to alleviate Doxorubicin-induced cardiotoxicity-induced ferroptosis and protect the myocardium. Epigallocatechin-3-gallate is a potential candidate phytochemical for combating Doxorubicin-induced cardiotoxicity.

REDOX BIOLOGY (2021)

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Review Pharmacology & Pharmacy

Nrf2 signaling pathway in cisplatin chemotherapy: Potential involvement in organ protection and chemoresistance

Sepideh Mirzaei et al.

Summary: Nrf2 signaling plays a crucial role in protecting against oxidative damage, but its activation in cancer cells can lead to chemoresistance. Modulating Nrf2 signaling during cisplatin treatment can suppress the development of chemoresistance and alleviate drug toxicity. Activating Nrf2 signaling can help prevent the side effects of cisplatin.

PHARMACOLOGICAL RESEARCH (2021)

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Article Biotechnology & Applied Microbiology

ROS-responsive liposomes with NIR light-triggered doxorubicin release for combinatorial therapy of breast cancer

Hanxi Yi et al.

Summary: Lipo/pB-DOX/ICG is a novel tool for on-demand drug release at tumor sites and a promising candidate for controllable and accurate combinatorial tumor therapy.

JOURNAL OF NANOBIOTECHNOLOGY (2021)

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Review Engineering, Biomedical

Organ-on-a-chip platforms for accelerating the evaluation of nanomedicine

Xi Chen et al.

Summary: Nanomedicine involves the use of nanoscale materials in diagnostic and therapeutic applications, with challenges in clinical translation due to difficulty in understanding nanomaterial behaviors in human environments. Organ Chip technology offers a promising solution by enabling in vitro simulation of in vivo microenvironments for robust evaluation of nanomedicine.

BIOACTIVE MATERIALS (2021)

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Article Medicine, Research & Experimental

Shenmai injection improves doxorubicin cardiotoxicity via miR-30a/Beclin 1

Xiaonan Zhang et al.

Summary: The study used network pharmacology methods to explore the potential mechanism of Shenmai Injection (SMI) in treating cardiotoxicity caused by anthracyclines. In a rat model, SMI was found to inhibit excessive myocardial autophagy by regulating the expression of miR-30a/Beclin 1, thus alleviating doxorubicin-induced myocardial injury.

BIOMEDICINE & PHARMACOTHERAPY (2021)

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Article Cardiac & Cardiovascular Systems

Dose-Dependent Cardioprotective Effect of Hemin in Doxorubicin-Induced Cardiotoxicity Via Nrf-2/HO-1 and TLR-5/NF-κB/TNF-α Signaling Pathways

Marwa M. M. Refaie et al.

Summary: The study demonstrated that hemin can reduce doxorubicin-induced cardiotoxicity in rats by modulating specific signaling pathways, with antioxidant, anti-inflammatory, and anti-apoptotic effects in a dose-dependent manner.

CARDIOVASCULAR TOXICOLOGY (2021)

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Article Biochemistry & Molecular Biology

Geraniol isolated from lemon grass to mitigate doxorubicin-induced cardiotoxicity through Nrf2 and NF-κB signaling

Nancy S. Younis et al.

Summary: Geraniol was found to have a protective effect against doxorubicin-induced cardiotoxicity, possibly through upregulating the expression of Nrf2 and HO-1, enhancing antioxidant capacity, and suppressing inflammation factors.

CHEMICO-BIOLOGICAL INTERACTIONS (2021)

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Article Immunology

Pinocembrin inhibited cardiomyocyte pyroptosis against doxorubicin-induced cardiac dysfunction via regulating Nrf2/Sirt3 signaling pathway

Jiwei Gu et al.

Summary: The study demonstrated that pinocembrin can significantly improve cardiac function, reduce cardiac fibrosis, and inhibit DOX-induced cardiomyocyte pyroptosis through activation of the Nrf2/Sirt3 signal pathway. This suggests that pinocembrin has potential therapeutic effects in protecting the heart from DOX-induced cardiotoxicity.

INTERNATIONAL IMMUNOPHARMACOLOGY (2021)

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Article Cardiac & Cardiovascular Systems

Wogonin Alleviates Cisplatin-induced Cardiotoxicity in Mice Via Inhibiting Gasdermin D-mediated Pyroptosis

Jiajun Xu et al.

Summary: Wogonin shows promise in mitigating CDDP-induced cardiotoxicity by protecting against cardiac dysfunction, myocardial injury, and pyroptosis. It also exhibits antipyroptotic effects by modulating the Gasdermin D protein, which could be beneficial for treating other diseases.

JOURNAL OF CARDIOVASCULAR PHARMACOLOGY (2021)

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Article Oncology

Advances in the application of nanotechnology in reducing cardiotoxicity induced by cancer chemotherapy

Xin Su et al.

SEMINARS IN CANCER BIOLOGY (2021)

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Article Medicine, Research & Experimental

Benazepril hydrochloride protects against doxorubicin cardiotoxicity by regulating the PI3K/Akt pathway

Lan Zhan et al.

Summary: Doxorubicin induces oxidative stress and apoptosis in cardiac cells, but benazepril hydrochloride can mitigate these effects by suppressing apoptosis through the PI3K/Akt signaling pathway. Treatment with benazepril-HCl may serve as an adjuvant therapy in reducing Doxorubicin-induced cardiotoxicity.

EXPERIMENTAL AND THERAPEUTIC MEDICINE (2021)

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Article Medicine, General & Internal

Loss of TRIM21 alleviates cardiotoxicity by suppressing ferroptosis induced by the chemotherapeutic agent doxorubicin

Kai Hou et al.

Summary: The study demonstrates that TRIM21 knockout protects against doxorubicin-induced cardiotoxicity in both doxorubicin treatment model and LAD model. Mechanistically, TRIM21 can protect the heart from ferroptosis by enhancing the sequestration of Keap1 by p62.

EBIOMEDICINE (2021)

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Article Biochemistry & Molecular Biology

Nerolidol Attenuates Oxidative Stress, Inflammation, and Apoptosis by Modulating Nrf2/MAPK Signaling Pathways in Doxorubicin-Induced Acute Cardiotoxicity in Rats

Seenipandi Arunachalam et al.

Summary: This study investigated the cardioprotective effects of nerolidol in a rat model of doxorubicin-induced acute cardiotoxicity, highlighting its antioxidant, anti-inflammatory, and antiapoptotic activities through modulation of cellular signaling pathways.

ANTIOXIDANTS (2021)

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Review Engineering, Biomedical

Organ-on-a-chip platforms for evaluation of environmental nanoparticle toxicity

Rick Xing Ze Lu et al.

Summary: Nanoparticles have raised concerns due to potential adverse health effects, necessitating the development of physiologically relevant models for toxicity assessment. Organ-on-a-chip models offer a new avenue for nanotoxicological research by recapitulating in vivo microenvironment and responses.

BIOACTIVE MATERIALS (2021)

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Article Pharmacology & Pharmacy

Targeted delivery by pH-responsive mPEG-S-PBLG micelles significantly enhances the anti-tumor efficacy of doxorubicin with reduced cardiotoxicity

Qiyi Feng et al.

Summary: Stimuli-responsive nanotherapeutics based on pH-responsive micelles showed great potential in precision oncology. The micelles efficiently encapsulated and released anti-cancer drugs, leading to cell death in cancer cells. They also prolonged blood circulation, reduced cardiac toxicity, and selectively delivered drugs to tumor tissues. Overall, these micelles significantly improved anti-tumor efficacy and reduced systemic toxicity, indicating their translational potential in precise drug delivery for cancer treatment.

DRUG DELIVERY (2021)

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Review Integrative & Complementary Medicine

Breviscapine: A Review on its Phytochemistry, Pharmacokinetics and Therapeutic Effects

Luan Wen et al.

Summary: Breviscapine is an extract of several flavonoids, with scutellarin as the main active component, showing a broad spectrum of pharmacological activities for treating cardiovascular and cerebrovascular diseases. Scutellarin and its analogs hold significant value in drug research and development.

AMERICAN JOURNAL OF CHINESE MEDICINE (2021)

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Review Biochemistry & Molecular Biology

Potential of exosomes as diagnostic biomarkers and therapeutic carriers for doxorubicin-induced

Chao Tian et al.

Summary: Doxorubicin is effective in cancer treatment but can cause cardiotoxicity. Exosomes serve as potential diagnostic markers for doxorubicin-induced cardiotoxicity and as carriers for drug delivery.

INTERNATIONAL JOURNAL OF BIOLOGICAL SCIENCES (2021)

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Article Biochemistry & Molecular Biology

Enhanced antitumor efficacy and attenuated cardiotoxicity of doxorubicin in combination with lycopene liposomes

Jinfang Zhu et al.

JOURNAL OF LIPOSOME RESEARCH (2020)

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Review Cell Biology

Modulatory effects of statins on the autophagy: A therapeutic perspective

Milad Ashrafizadeh et al.

JOURNAL OF CELLULAR PHYSIOLOGY (2020)

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Review Oncology

Major obstacles to doxorubicin therapy: Cardiotoxicity and drug resistance

Hamdan S. Al-malky et al.

JOURNAL OF ONCOLOGY PHARMACY PRACTICE (2020)

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Article Medicine, Research & Experimental

Cardamonin protects against doxorubicin-induced cardiotoxicity in mice by restraining oxidative stress and inflammation associated with Nrf2 signaling

Wang Qi et al.

BIOMEDICINE & PHARMACOTHERAPY (2020)

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Article Medicine, Research & Experimental

Magnoflorine improves sensitivity to doxorubicin (DOX) of breast cancer cells via inducing apoptosis and autophagy through AKT/mTOR and p38 signaling pathways

Tian Wei et al.

BIOMEDICINE & PHARMACOTHERAPY (2020)

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Article Plant Sciences

Glycyrrhiza glabra (Licorice) root extract attenuates doxorubicin-induced cardiotoxicity via alleviating oxidative stress and stabilising the cardiac health in H9c2 cardiomyocytes

Shishir Upadhyay et al.

JOURNAL OF ETHNOPHARMACOLOGY (2020)

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Article Medicine, Research & Experimental

Bnip3 mediates doxorubicin-induced cardiomyocyte pyroptosis via caspase-3/GSDME

Xinbin Zheng et al.

LIFE SCIENCES (2020)

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Article Chemistry, Medicinal

Calycosin ameliorates doxorubicin-induced cardiotoxicity by suppressing oxidative stress and inflammation via the sirtuin 1-NOD-like receptor protein 3 pathway

Jinghui Zhai et al.

PHYTOTHERAPY RESEARCH (2020)

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Article Cardiac & Cardiovascular Systems

Reactive fibrosis precedes doxorubicin-induced heart failure through sterile inflammation

Ryo Tanaka et al.

ESC HEART FAILURE (2020)

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Article Pharmacology & Pharmacy

Dihydromyricetin alleviates doxorubicin-induced cardiotoxicity by inhibiting NLRP3 inflammasome through activation of SIRT1

Zhenzhu Sun et al.

BIOCHEMICAL PHARMACOLOGY (2020)

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Article Biochemistry & Molecular Biology

Protective effect of curcumin nanoparticles against cardiotoxicity induced by doxorubicin in rat

Haitham S. Mohammed et al.

BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE (2020)

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Article Oncology

TFEB-NF-κB inflammatory signaling axis: a novel therapeutic pathway of Dihydrotanshinone I in doxorubicin-induced cardiotoxicity

Xiaoping Wang et al.

JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH (2020)

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Article Biotechnology & Applied Microbiology

Sinapic Acid Ameliorates Oxidative Stress, Inflammation, and Apoptosis in Acute Doxorubicin-Induced Cardiotoxicity via the NF-κB-Mediated Pathway

Yousef A. Bin Jardan et al.

BIOMED RESEARCH INTERNATIONAL (2020)

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Article Toxicology

Effect of co-treatment with doxorubicin and verapamil loaded into chitosan nanoparticles on diethylnitrosamine-induced hepatocellular carcinoma in mice

H. E. Abo Mansour et al.

HUMAN & EXPERIMENTAL TOXICOLOGY (2020)

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Article Cardiac & Cardiovascular Systems

Disruption of the Keap1/Nrf2-Antioxidant Response System After Chronic Doxorubicin Exposure In Vivo

Kendra K. S. Nordgren et al.

CARDIOVASCULAR TOXICOLOGY (2020)

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Article Immunology

Crocin protects against cardiotoxicity induced by doxorubicin through TLR-2/NF-κB signal pathway in vivo and vitro

Xi Chu et al.

INTERNATIONAL IMMUNOPHARMACOLOGY (2020)

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Article Cell Biology

TLR9 deficiency alleviates doxorubicin-induced cardiotoxicity via the regulation of autophagy

Zhen Guo et al.

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE (2020)

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Article Medicine, Research & Experimental

Mitochondria-dependent ferroptosis plays a pivotal role in doxorubicin cardiotoxicity

Tomonori Tadokoro et al.

JCI INSIGHT (2020)

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Article Medicine, Research & Experimental

Yangxin granules alleviate doxorubicin-induced cardiotoxicity by suppressing oxidative stress and apoptosis mediated by AKT/GSK3<bold>beta</bold>/<bold>beta</bold>-catenin signaling

Dezhi Ren et al.

JOURNAL OF INTERNATIONAL MEDICAL RESEARCH (2020)

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Article Medicine, Research & Experimental

NF-κB pathway activation during endothelial-to-mesenchymal transition in a rat model of doxorubicin-induced cardiotoxicity

Anji Xu et al.

BIOMEDICINE & PHARMACOTHERAPY (2020)

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Article Biochemistry & Molecular Biology

BAY60-2770 attenuates doxorubicin-induced cardiotoxicity by decreased oxidative stress and enhanced autophagy

Xiao-Xiao Zhao et al.

CHEMICO-BIOLOGICAL INTERACTIONS (2020)

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Article Pharmacology & Pharmacy

Glycyrrhizin improved autophagy flux via HMGB1-dependent Akt/mTOR signaling pathway to prevent Doxorubicin-induced cardiotoxicity

Xueli Lv et al.

TOXICOLOGY (2020)

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Article Cell Biology

Doxorubicin cardiomyopathy is ameliorated by acacetin via Sirt1-mediated activation of AMPK/Nrf2 signal molecules

Wei-Yin Wu et al.

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE (2020)

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Article Oncology

Cathepsin B aggravated doxorubicin-induced myocardial injury via NF-κB signalling

Chen Liu et al.

MOLECULAR MEDICINE REPORTS (2020)

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Article Cell Biology

Acyl-CoA thioesterase 1 prevents cardiomyocytes from Doxorubicin-induced ferroptosis via shaping the lipid composition

Yunchang Liu et al.

CELL DEATH & DISEASE (2020)

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Article Biotechnology & Applied Microbiology

Orosomucoid 1 Attenuates Doxorubicin-Induced Oxidative Stress and Apoptosis in Cardiomyocytes via Nrf2 Signaling

Xiaoli Cheng et al.

BIOMED RESEARCH INTERNATIONAL (2020)

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Article Biochemistry & Molecular Biology

Meteorin-like protein attenuates doxorubicin-induced cardiotoxicity via activating cAMP/PKA/SIRT1 pathway

Can Hu et al.

REDOX BIOLOGY (2020)

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Article Cardiac & Cardiovascular Systems

Curcumin suppresses doxorubicin-induced cardiomyocyte pyroptosis via a PI3K/Akt/mTOR-dependent manner

Wei Yu et al.

CARDIOVASCULAR DIAGNOSIS AND THERAPY (2020)

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Article Nanoscience & Nanotechnology

Fluorescent Magnetic Iron Oxide Nanoparticle-Encapsulated Protein Hydrogel Against Doxorubicin-Associated Cardiotoxicity and for Enhanced Cardiomyocyte Survival

Pingshuan Dong et al.

JOURNAL OF BIOMEDICAL NANOTECHNOLOGY (2020)

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Article Biotechnology & Applied Microbiology

Exosomal LncRNA-NEAT1 derived from MIF-treated mesenchymal stem cells protected against doxorubicin-induced cardiac senescence through sponging miR-221-3p

Lei Zhuang et al.

JOURNAL OF NANOBIOTECHNOLOGY (2020)

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Article Cardiac & Cardiovascular Systems

Micheliolide Protects Against Doxorubicin-Induced Cardiotoxicity in Mice by Regulating PI3K/Akt/NF-kB Signaling Pathway

Ashkan Kalantary-Charvadeh et al.

CARDIOVASCULAR TOXICOLOGY (2019)

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Article Food Science & Technology

Wheat phenolics suppress doxorubicin-induced cardiotoxicity via inhibition of oxidative stress, MAP kinase activation, NF-κB pathway, PI3K/Akt/mTOR impairment, and cardiac apoptosis

Ranabir Sahu et al.

FOOD AND CHEMICAL TOXICOLOGY (2019)

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Article Pharmacology & Pharmacy

Irbesartan suppresses cardiac toxicity induced by doxorubicin via regulating the p38-MAPK/NF-κB and TGF-β1 pathways

Nermin T. El-Said et al.

NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY (2019)

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Review Pharmacology & Pharmacy

The Effects of Breviscapine Injection on Hypertension in Hypertension-Induced Renal Damage Patients: A Systematic Review and a Meta-Analysis

Lihua Wu et al.

FRONTIERS IN PHARMACOLOGY (2019)

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Article Medicine, Research & Experimental

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ACS BIOMATERIALS SCIENCE & ENGINEERING (2019)

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Resveratrol solid lipid nanoparticles to trigger credible inhibition of doxorubicin cardiotoxicity

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INTERNATIONAL JOURNAL OF NANOMEDICINE (2019)

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Yellow Wine Polyphenolic Compounds prevents Doxorubicin-induced cardiotoxicity through activation of the Nrf2 signalling pathway

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MicroRNA-128-3p aggravates doxorubicin-induced liver injury by promoting oxidative stress via targeting Sirtuin-1

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PGC1α activation by pterostilbene ameliorates acute doxorubicin cardiotoxicity by reducing oxidative stress via enhancing AMPK and SIRT1 cascades

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CD-340 functionalized doxorubicin-loaded nanoparticle induces apoptosis and reduces tumor volume along with drug-related cardiotoxicity in mice

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Doxorubicin induces cardiomyocyte pyroptosis via the TINCR-mediated posttranscriptional stabilization of NLR family pyrin domain containing 3

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miR-200a Attenuated Doxorubicin-Induced Cardiotoxicity through Upregulation of Nrf2 in Mice

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Exosome Treatment Enhances Anti-Inflammatory M2 Macrophages and Reduces Inflammation-Induced Pyroptosis in Doxorubicin-Induced Cardiomyopathy

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p-Coumaric acid mediated protection of H9c2 cells from Doxorubicininduced cardiotoxicity: Involvement of augmented Nrf2 and autophagy

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Nanoceria ameliorates doxorubicin induced cardiotoxicity: Possible mitigation via reduction of oxidative stress and inflammation

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Apremilast prevent doxorubicin-induced apoptosis and inflammation in heart through inhibition of oxidative stress mediated activation of NF-κB signaling pathways

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Protective effect of dioscin against doxorubicin-induced cardiotoxicity via adjusting microRNA-140-5p-mediated myocardial oxidative stress

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MicroRNA-140-5p aggravates doxorubicin-induced cardiotoxicity by promoting myocardial oxidative stress via targeting Nrf2 and Sirt2

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Curcumin attenuates doxorubicin-induced cardiotoxicity via suppressing oxidative stress and preventing mitochondrial dysfunction mediated by 14-3-3γ

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Ginsenoside Rg1 Prevents Doxorubicin-Induced Cardiotoxicity through the Inhibition of Autophagy and Endoplasmic Reticulum Stress in Mice

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Apremilast prevent doxorubicin-induced apoptosis and inflammation in heart through inhibition of oxidative stress mediated activation of NF-κB signaling pathways

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Polyphenols, autophagy and doxorubicin-induced cardiotoxicity

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Liraglutide ameliorates cardiotoxicity induced by doxorubicin in rats through the Akt/GSK-3β signaling pathway

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TRENDS IN BIOCHEMICAL SCIENCES (2017)

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Review Pharmacology & Pharmacy

Therapeutic Effects of Breviscapine in Cardiovascular Diseases: A Review

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Mechanistic clues to the protective effect of chrysin against doxorubicin-induced cardiomyopathy: Plausible roles of p53, MAPK and AKT pathways

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Review Biochemistry & Molecular Biology

Ferroptosis: A Regulated Cell Death Nexus Linking Metabolism, Redox Biology, and Disease

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Protection of Luteolin-7-O-Glucoside Against Doxorubicin-Induced Injury Through PTEN/Akt and ERK Pathway in H9c2 Cells

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Article Pharmacology & Pharmacy

JAK2/STAT3 Pathway Mediates Protection of Metallothionein Against Doxorubicin-Induced Cytotoxicity in Mouse Cardiomyocytes

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INTERNATIONAL JOURNAL OF TOXICOLOGY (2016)

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Gp130-mediated STAT3 activation by S-propargyl-cysteine, an endogenous hydrogen sulfide initiator, prevents doxorubicin-induced cardiotoxicity

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Ginkgolide B Exerts Cardioprotective Properties against Doxorubicin-Induced Cardiotoxicity by Regulating Reactive Oxygen Species, Akt and Calcium Signaling Pathways In Vitro and In Vivo

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FL3, a Synthetic Flavagline and Ligand of Prohibitins, Protects Cardiomyocytes via STAT3 from Doxorubicin Toxicity

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Astragalus Polysaccharide Suppresses Doxorubicin-Induced Cardiotoxicity by Regulating the PI3k/Akt and p38MAPK Pathways

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Ferroptosis: An Iron-Dependent Form of Nonapoptotic Cell Death

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Adiponectin Ameliorates Doxorubicin-induced Cardiotoxicity through Akt Protein-dependent Mechanism

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Pathology of late-onset anthracycline cardiomyopathy

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Heat Shock Protein 20 Interacting With Phosphorylated Akt Reduces Doxorubicin-Triggered Oxidative Stress and Cardiotoxicity

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Endothelial-to-mesenchymal transition contributes to cardiac fibrosis

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DP Bartel

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Increasing dose intensity of anthracycline antibiotics improves outcome in patients with acute myelogenous leukemia

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Safety and activity of the combination of pegylated liposomal doxorubicin and weekly docetaxel in advanced breast cancer

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Adriamycin-induced heart failure: mechanisms and modulation

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