坏死性上睑下垂：心血管疾病干预的重要和有前途的目标

IF 5.3 2区医学 Q1 PHARMACOLOGY & PHARMACY

Biochemical pharmacology Pub Date : 2025-04-21 DOI:10.1016/j.bcp.2025.116951

Yan-wei Ji , Xin-yu Wen , He-peng Tang , Wa-ting Su, Zhong-yuan Xia, Shao-qing Lei

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引用次数: 0

摘要

由于饮食结构的变化、人口老龄化和代谢危险因素的加剧，心血管疾病的发病率每年都在持续上升，在世界范围内构成了重大的健康负担。细胞死亡在心血管疾病的发生和发展中起着至关重要的作用。作为细胞在不利应激条件下遇到的一个受调节的终点，坏死性上睑衰竭的执行受经典途径、钙调素依赖性蛋白激酶（CaMK）途径和线粒体依赖性途径的调节，并与各种心血管疾病有关，包括动脉粥样硬化、心肌梗死、心肌缺血-再灌注损伤（IRI）、心力衰竭、糖尿病性心肌病、扩张型心肌病、肥厚性心肌病、心肌病、动脉粥样硬化、动脉粥样硬化、动脉粥样硬化、动脉粥样硬化、动脉粥样硬化、动脉粥样硬化和动脉粥样硬化。化疗药物性心肌病，腹主动脉瘤（AAA）。为了进一步研究心血管疾病的潜在治疗靶点，我们还分析了与坏死性上睑下垂有关的主要分子及其抑制剂，以努力揭示治疗的见解。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

Necroptosis: a significant and promising target for intervention of cardiovascular disease

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Necroptosis: a significant and promising target for intervention of cardiovascular disease

Due to changes in dietary structures, population aging, and the exacerbation of metabolic risk factors, the incidence of cardiovascular disease continues to rise annually, posing a significant health burden worldwide. Cell death plays a crucial role in the onset and progression of cardiovascular diseases. As a regulated endpoint encountered by cells under adverse stress conditions, the execution of necroptosis is regulated by classicalpathways, the calmodulin-dependent protein kinases (CaMK) pathway, and mitochondria-dependent pathways, and implicated in various cardiovascular diseases, including atherosclerosis, myocardial infarction, myocardial ischemia–reperfusion injury (IRI), heart failure, diabetic cardiomyopathy, dilated cardiomyopathy, hypertrophic cardiomyopathy, chemotherapy drug-induced cardiomyopathy, and abdominal aortic aneurysm (AAA). To further investigate potential therapeutic targets for cardiovascular diseases, we also analyzed the main molecules and their inhibitors involved in necroptosis in an effort to uncover insights for treatment.

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来源期刊

Biochemical pharmacology 医学-药学

CiteScore

10.30

自引率

1.70%

发文量

420

审稿时长

17 days

期刊介绍： Biochemical Pharmacology publishes original research findings, Commentaries and review articles related to the elucidation of cellular and tissue function(s) at the biochemical and molecular levels, the modification of cellular phenotype(s) by genetic, transcriptional/translational or drug/compound-induced modifications, as well as the pharmacodynamics and pharmacokinetics of xenobiotics and drugs, the latter including both small molecules and biologics. The journal''s target audience includes scientists engaged in the identification and study of the mechanisms of action of xenobiotics, biologics and drugs and in the drug discovery and development process. All areas of cellular biology and cellular, tissue/organ and whole animal pharmacology fall within the scope of the journal. Drug classes covered include anti-infectives, anti-inflammatory agents, chemotherapeutics, cardiovascular, endocrinological, immunological, metabolic, neurological and psychiatric drugs, as well as research on drug metabolism and kinetics. While medicinal chemistry is a topic of complimentary interest, manuscripts in this area must contain sufficient biological data to characterize pharmacologically the compounds reported. Submissions describing work focused predominately on chemical synthesis and molecular modeling will not be considered for review. While particular emphasis is placed on reporting the results of molecular and biochemical studies, research involving the use of tissue and animal models of human pathophysiology and toxicology is of interest to the extent that it helps define drug mechanisms of action, safety and efficacy.