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Recent Advances in Mitochondrial Fission/Fusion-Targeted Therapy in Doxorubicin-Induced Cardiotoxicity

PHARMACEUTICS (2023)

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Summary: Each year, the American Cancer Society compiles data on cancer occurrence and outcomes in the United States. The latest data shows that breast and prostate cancer progress has stagnated, while lung cancer has shown improvements in survival rates. Lung cancer incidence for advanced disease has declined while localized-stage rates have increased, resulting in higher survival rates. Mortality patterns align with incidence trends, with lung cancer deaths declining rapidly, breast cancer deaths slowing, and prostate cancer deaths stabilizing.

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Mitochondrial-Targeted Therapy for Doxorubicin-Induced Cardiotoxicity

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Summary: This article reviews the pathogenic mechanisms of doxorubicin-induced cardiotoxicity and presents updated cardioprotective strategies. The focus of the research is on protecting mitochondria, covering different therapeutic modalities, and exploring advances in using stem cells as a research platform.

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Acetylcholine receptor agonists provide cardioprotection in doxorubicin-induced cardiotoxicity via modulating muscarinic M2 and a7 nicotinic receptor expression

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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.

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

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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.

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Mfn2-mediated mitochondrial fusion alleviates doxorubicin-induced cardiotoxicity with enhancing its anticancer activity through metabolic switch

Mingge Ding et al.

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The Impairment of Cell Metabolism by Cardiovascular Toxicity of Doxorubicin Is Reversed by Bergamot Polyphenolic Fraction Treatment in Endothelial Cells

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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.

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The Role of Mitochondrial Quality Control in Anthracycline-Induced Cardiotoxicity: From Bench to Bedside

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Summary: Cardiotoxicity is a major side effect of anthracycline chemotherapy drugs, and the loss of mitochondrial quality control appears to play a crucial role in its development. Restoring the cardiomyocyte's mitochondrial quality control system may have therapeutic potential in preventing and intervening in cardiotoxicity.

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Remote ischaemic preconditioning ameliorates anthracycline-induced cardiotoxicity and preserves mitochondrial integrity

Carlos Galan-Arriola et al.

Summary: This study demonstrates that RIPC applied immediately before each doxorubicin injection can preserve cardiac contractility, result in significantly higher long-term left ventricular ejection fraction, and less cardiac fibrosis in a translatable large-animal model of AIC. RIPC is able to prevent mitochondrial fragmentation and dysregulated autophagy from AIC early stages, suggesting it as a promising intervention for testing in clinical trials for AIC.

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Advances in Cardiotoxicity Induced by Altered Mitochondrial Dynamics and Mitophagy

Yiyuan Yin et al.

Summary: Mitochondria play a crucial role in maintaining normal cardiac function, but continuous damage can disrupt the balance of mitochondrial dynamics and mitophagy, leading to energy supply disorders and toxic accumulation in cardiac cells, ultimately resulting in cardiac damage and toxicity. This review highlights the importance of oxidative stress in mitophagy and aims to provide insights for preventing and treating cardiotoxicity caused by altered mitochondrial dynamics and mitophagy.

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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.

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Acetylcholinesterase inhibitor ameliorates doxorubicin-induced cardiotoxicity through reducing RIP1-mediated necroptosis

Thawatchai Khuanjing et al.

Summary: The study showed that donepezil can alleviate doxorubicin-induced cardiotoxicity, reduce cardiac damage, and improve cardiac function.

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Neuraminidase1 Inhibitor Protects Against Doxorubicin-Induced Cardiotoxicity via Suppressing Drp1-Dependent Mitophagy

Yating Qin et al.

Summary: Anthracyclines like doxorubicin are effective chemotherapeutic drugs but limited by irreversible cardiotoxicity. This study investigated NEU1's role in doxorubicin-induced cardiomyopathy and the protective effects of NEU1 inhibitor oseltamivir. Results showed NEU1 as a crucial inducer of doxorubicin-induced cardiomyopathy by promoting Drp1-dependent mitochondrial fission and mitophagy, with NEU1 inhibitor showing new cardio-protection indications against doxorubicin cardiotoxicity.

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Ana Reis-Mendes et al.

Summary: This study investigated the effects of doxorubicin (DOX) on infant and adult mice, revealing that adult mice were more susceptible to DOX-induced cardiotoxicity due to inflammation, while infant mice seemed to be protected by activating antioxidant defenses like Nrf2.

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Klotho attenuated Doxorubicin-induced cardiomyopathy by alleviating Dynamin-related protein 1-mediated mitochondrial dysfunction

Xiaodong Zhuang et al.

Summary: This study revealed that Klotho alleviated Dox-induced cardiotoxicity by reducing apoptosis and mitochondrial fission through down-regulating Drp1 expression, highlighting new targets for the therapy of Dox-induced cardiomyopathy.

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Targeting Oxidative Stress, NLRP3 Inflammasome, and Autophagy by Fraxetin to Combat Doxorubicin-Induced Cardiotoxicity

Ahmed M. Kabel et al.

Summary: The study found that fraxetin can mitigate the harmful effects of oxidative stress and inflammation on myocardial muscles in a dose-dependent manner, decrease NLRP3 inflammasome, enhance autophagy, and improve apoptotic signaling pathways. Additionally, fraxetin can counteract the echocardiographic, histopathological, immunohistochemical, and electron microscopic changes induced by doxorubicin in cardiomyocytes in a dose-dependent manner.

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Article Cardiac & Cardiovascular Systems

Luteolin Prevents Cardiac Dysfunction and Improves the Chemotherapeutic Efficacy of Doxorubicin in Breast Cancer

Youyang Shi et al.

Summary: Luteolin can mitigate Doxorubicin-induced toxicity in cardiomyocytes by reducing oxidative stress, decreasing mitochondrial fission, and lowering levels of apoptosis. In addition, Luteolin exhibits protective effects in zebrafish and enhances the cytotoxicity of Doxorubicin in triple-negative breast cancer by inhibiting proliferation, metastasis, and inducing apoptosis.

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Review Cell Biology

Regulated cell death pathways in doxorubicin-induced cardiotoxicity

Effimia Christidi et al.

Summary: This review summarizes recent advances in understanding the mechanisms by which Doxorubicin induces cardiomyocyte death, including pathways such as autophagy, ferroptosis, necroptosis, pyroptosis, and apoptosis. Understanding these mechanisms may help identify novel therapeutic agents and lead to more targeted approaches to cardiotoxicity testing.

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N-Alkylation of Anthracycline Antibiotics by Natural Sesquiterpene Lactones as a Way to Obtain Antitumor Agents with Reduced Side Effects

Margarita Neganova et al.

Summary: The combination of anthracycline antibiotics with natural sesquiterpene lactones shows promising results in terms of cytotoxicity and glycolysis inhibition, while reducing damaging effects on rat heart mitochondria. This strategy may lead to the development of potential antitumor chemotherapeutic drugs with enhanced efficacy against tumor cells and reduced toxicity to healthy cells.

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Early treatment with combination of SS31 and entresto effectively preserved the heart function in doxorubicin-induced dilated cardiomyopathic rat

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Luteolin Attenuates Doxorubicin-Induced Cardiotoxicity Through Promoting Mitochondrial Autophagy

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Shenmai Injection Protects Against Doxorubicin-Induced Cardiotoxicity via Maintaining Mitochondrial Homeostasis

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Mitophagy inhibitor liensinine suppresses doxorubicin-induced cardiotoxicity through inhibition of Drp1-mediated maladaptive mitochondrial fission

Xinyue Liang et al.

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Inhibition of miR-23a attenuates doxorubicin-induced mitochondria-dependent cardiomyocyte apoptosis by targeting the PGC-1α/Drp1 pathway

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