☆ 4.3 Article

TBC1 domain family member 25 protects against myocardial apoptosis and the proinflammatory response triggered by ischemia-reperfusion injury through suppression of the TAK1-JNK/p38 MAPK signaling cascade

IN VITRO CELLULAR & DEVELOPMENTAL BIOLOGY-ANIMAL (2023)

Related references

Note: Only part of the references are listed.

Article Cell Biology

TBC1D25 alleviates nonalcoholic steatohepatitis by inhibiting abnormal lipid accumulation and inflammation

Anding Wu et al.

Summary: Nonalcoholic fatty liver disease (NAFLD) is a significant contributor to cardiovascular diseases, affecting a quarter of the global population. This study revealed that the expression of TBC1 domain family member 25 (TBC1D25) is upregulated in NAFLD/NASH. TBC1D25 deficiency worsened hepatic steatosis, inflammation, and fibrosis in NASH, while its overexpression inhibited NASH responses.

JOURNAL OF CELLULAR PHYSIOLOGY (2023)

Add to Collection

Review Chemistry, Multidisciplinary

Recent advances in nanomedicines for imaging and therapy of myocardial ischemia-reperfusion injury

Jingjing Wang et al.

Summary: Myocardial ischemia-reperfusion injury (IRI) is a common cardiovascular disease caused by the restoration of blood flow to the ischemic myocardium. Nanomedicines have shown great potential in the diagnosis and treatment of myocardial IRI due to their advantageous properties. This review focuses on the rational design of nanomedicines for optimal imaging and therapy of myocardial IRI.

JOURNAL OF CONTROLLED RELEASE (2023)

Add to Collection

Article Chemistry, Multidisciplinary

Notoginsenoside R1 protects against myocardial ischemia/reperfusion injury in mice via suppressing TAK1-JNK/p38 signaling

Jing-jing Zeng et al.

Summary: This study investigated the cardioprotective mechanisms of notoginsenoside R1 (NG-R1) in myocardial ischemia/reperfusion (MI/R) injury. The results showed that administration of NG-R1 significantly reduced myocardial infarction area, alleviated myocardial cell damage, and improved cardiac function in MI/R mice. The study also revealed that NG-R1 inhibited apoptosis in cardiomyocytes by suppressing TAK1, JNK, and p38 signaling.

ACTA PHARMACOLOGICA SINICA (2023)

Add to Collection

Article Integrative & Complementary Medicine

Research Progress of Chinese Medicine in the Treatment of Myocardial Ischemia-Reperfusion Injury

Li Dong et al.

Summary: Vascular recanalization is essential in diagnosing severe coronary artery stenosis, but it can lead to myocardial ischemia-reperfusion injury. Traditional Chinese medicine has shown strong vitality in MIRI therapy, with multiple-target effects including anti-inflammatory, antioxidant, and cardio-protection effects.

AMERICAN JOURNAL OF CHINESE MEDICINE (2023)

Add to Collection

Article Cardiac & Cardiovascular Systems

Heart Disease and Stroke Statistics-2023 Update: A Report From the American Heart Association

Connie W. Tsao et al.

Summary: The American Heart Association, in collaboration with the National Institutes of Health, releases annual statistics on heart disease, stroke, and cardiovascular risk factors. The Statistical Update provides the latest data on various heart and circulatory diseases and their outcomes, as well as information on core health behaviors and factors contributing to cardiovascular health.

CIRCULATION (2023)

Add to Collection

Article Biochemistry & Molecular Biology

TBC1Domain Family Member 25 deficiency aggravates cerebral ischemia-reperfusion injury via TAK1-JNK/p38 pathway

Zongyong Zhang et al.

Summary: TBC1Domain Family Member 25 (TBC1D25) plays a crucial role in brain ischemia-reperfusion (I/R) injury, with its deficiency exacerbating neuronal loss, apoptosis, and inflammation. The protective mechanism of TBC1D25 relies on the regulation of the TAK1-JNK/p38 signaling pathway.

JOURNAL OF NEUROCHEMISTRY (2022)

Add to Collection

Review Cardiac & Cardiovascular Systems

Promising Therapeutic Candidate for Myocardial Ischemia/Reperfusion Injury: What Are the Possible Mechanisms and Roles of Phytochemicals?

Cong Chen et al.

Summary: Percutaneous coronary intervention (PCI) is an effective reperfusion strategy for acute myocardial infarction (AMI), but it can cause myocardial ischemia/reperfusion (I/R) injury. Myocardial I/R injury leads to cardiomyocyte death and increases the risk of infarct size and heart failure. Phytochemicals derived from Chinese herbal medicine have shown potential cardioprotective effects against myocardial I/R injury and deserve further investigation.

FRONTIERS IN CARDIOVASCULAR MEDICINE (2022)

Add to Collection

Review Immunology

Potential therapeutic strategies for myocardial infarction: the role of Toll-like receptors

Sumra Komal et al.

Summary: Myocardial infarction is a life-threatening condition with a high incidence and mortality rate worldwide. Understanding the genetic and epigenetic factors involved in its development is crucial for early management and treatment. Toll-like receptors (TLRs) play a role in both adaptive and innate immunity, and their prolonged activation can lead to inflammation and contribute to the development of myocardial inflammation, MI, ischemia-reperfusion injury, myocarditis, and heart failure.

IMMUNOLOGIC RESEARCH (2022)

Add to Collection

Article Cell Biology

GCN5-mediated regulation of pathological cardiac hypertrophy via activation of the TAK1-JNK/p38 signaling pathway

Jia Li et al.

Summary: Pathological cardiac hypertrophy is a major risk factor for heart failure, characterized by abnormal remodeling of cardiomyocytes in response to pressure overload or other stress stimuli. The study reveals that GCN5 plays a significant role in promoting cardiac hypertrophy through excessive activation of the TAK1-JNK/p38 signaling pathway.

CELL DEATH & DISEASE (2022)

Add to Collection

Review Medicine, Research & Experimental

Myocardial ischemia/reperfusion injury: Mechanisms of injury and implications for management (Review)

Jianfeng He et al.

Summary: Myocardial infarction is a leading cause of death in patients with coronary heart disease worldwide. Myocardial ischemia/reperfusion injury (MIRI) results in more serious damage to the ischemic myocardium when the blood supply is restored. The mechanisms of MIRI involve oxidative stress, calcium overload, energy metabolism disorder, apoptosis, endoplasmic reticulum stress, autophagy, pyroptosis, necroptosis, and ferroptosis. Apoptosis and autophagy have received more attention, but necroptosis and ferroptosis also play important roles. However, the exact mechanism of MIRI remains unclear.

EXPERIMENTAL AND THERAPEUTIC MEDICINE (2022)

Add to Collection

Article Cardiac & Cardiovascular Systems

Research Progress on The Mechanism and Treatment of Inflammatory Response in Myocardial Ischemia-Reperfusion Injury

Dong Zhang et al.

Summary: The mechanism of inflammatory response after acute myocardial infarction and the clinical value and potential of inhibiting inflammatory response in the treatment of acute myocardial infarction are reviewed.

HEART SURGERY FORUM (2022)

Add to Collection

Article Cardiac & Cardiovascular Systems

Treatment strategies of acute myocardial infarction: updates on revascularization, pharmacological therapy, and beyond

Yuichi Saito et al.

Journal of Cardiology (2022)

Add to Collection

Review Cardiac & Cardiovascular Systems

N(6)-methyladenosine modification: A vital role of programmed cell death in myocardial ischemia/reperfusion injury

Jian Wang et al.

Summary: This review summarizes the regulators of m6A modification and their bioeffects on programmed cell death in myocardial ischemia/reperfusion injury.

INTERNATIONAL JOURNAL OF CARDIOLOGY (2022)

Add to Collection

Article Gastroenterology & Hepatology

Tripartite Motif-Containing 27 Attenuates Liver Ischemia/Reperfusion Injury by Suppressing Transforming Growth Factor β-Activated Kinase 1 (TAK1) by TAK1 Binding Protein 2/3 Degradation

San-Yang Chen et al.

Summary: TRIM27 plays a crucial role in hepatic I/R injury by mediating the degradation of TAB2/3 and suppression of downstream TAK1-JNK/p38 signaling, offering a promising approach to protect the liver from I/R-mediated damage.

HEPATOLOGY (2021)

Add to Collection

Article Cell Biology

RabGAP TBC1D25 is involved in human osteoclast activity

Michele Roy et al.

Summary: TBC1D25, a RabGAP identified in bone-resorbing osteoclasts, plays a role in bone resorption by regulating osteoclast polarization, absorption, and multinucleation. Inhibiting TBC1D25 expression decreases bone resorption and the formation of multinucleated cells.

EUROPEAN JOURNAL OF CELL BIOLOGY (2021)

Add to Collection

Article Genetics & Heredity

First evidence of involvement of TBC1D25 in causing human male infertility

Shoaib Nawaz et al.

Summary: Male infertility can result from disruption in molecular and cellular pathways involved in spermatogenesis. The involvement of the TBC1D25 gene in oligozoospermia in a family has been described for the first time, suggesting a possible role for the variant in causing male infertility.

EUROPEAN JOURNAL OF MEDICAL GENETICS (2021)

Add to Collection

Article Cardiac & Cardiovascular Systems

Dual-Specificity Phosphatase 26 Protects Against Cardiac Hypertrophy Through TAK1

Jing Zhao et al.

Summary: The study found that DUSP26 inhibits cardiac hypertrophy and protects the heart from pressure overload-induced hypertrophy by modulating the transforming growth factor-beta activated kinase 1-p38/c-Jun N-terminal kinase signaling pathway. Therefore, DUSP26 may serve as a therapeutic target for the treatment of cardiac hypertrophy and heart failure.

JOURNAL OF THE AMERICAN HEART ASSOCIATION (2021)

Add to Collection

Article Cell Biology

TAK1 signaling activity links the mast cell cytokine response and degranulation in allergic inflammation

Colton J. F. Watson et al.

JOURNAL OF LEUKOCYTE BIOLOGY (2020)

Add to Collection

Article Cell Biology

Inhibition of TGFβ-activated protein kinase 1 ameliorates myocardial ischaemia/reperfusion injury via endoplasmic reticulum stress suppression

Jingjing Zeng et al.

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE (2020)

Add to Collection

Review Cardiac & Cardiovascular Systems

Myocardial ischaemia-reperfusion injury and cardioprotection in perspective

Gerd Heusch

NATURE REVIEWS CARDIOLOGY (2020)

Add to Collection

Article Biochemistry & Molecular Biology

TBC1D25 Regulates Cardiac Remodeling Through TAK1 Signaling Pathway

Sen Guo et al.

INTERNATIONAL JOURNAL OF BIOLOGICAL SCIENCES (2020)

Add to Collection

Review Biochemistry & Molecular Biology

TAK1 mediates convergence of cellular signals for death and survival

Sabreena Aashaq et al.

APOPTOSIS (2019)

Add to Collection

Article Biochemistry & Molecular Biology

Tripartite Motif 8 Deficiency Relieves Hepatic Ischaemia/reperfusion Injury via TAK1-dependent Signalling Pathways

Qiu Tao et al.

INTERNATIONAL JOURNAL OF BIOLOGICAL SCIENCES (2019)

Add to Collection

Article Cell Biology

Differing susceptibility to autophagic degradation of two LC3-binding proteins: SQSTM1/p62 and TBC1D25/OATL1

Satoshi Hirano et al.

AUTOPHAGY (2016)

Add to Collection

Article Peripheral Vascular Disease

Mnk1 (Mitogen-Activated Protein Kinase-Interacting Kinase 1) Deficiency Aggravates Cardiac Remodeling in Mice

Yuan Yuan et al.

HYPERTENSION (2016)

Add to Collection

Article Cell Biology

Evolution of Tre-2/Bub2/Cdc16 (TBC) Rab GTPase-activating proteins

Carme Gabernet-Castello et al.

MOLECULAR BIOLOGY OF THE CELL (2013)

Add to Collection

Article Cell Biology

OATL1, a novel autophagosome-resident Rab33B-GAP, regulates autophagosomal maturation

Takashi Itoh et al.

JOURNAL OF CELL BIOLOGY (2011)

Add to Collection

© Peeref 2019-2024. All rights reserved.