程序性细胞死亡
GPX4
疾病
心肌病
医学
细胞内
生物
氧化应激
心力衰竭
细胞生物学
内科学
细胞凋亡
生物化学
谷胱甘肽过氧化物酶
过氧化氢酶
作者
Yang Zhang,Laiyun Xin,Mi Xiang,Chang Shang,Yuling Wang,Yan Wang,Xiangning Cui,Yingdong Lu
标识
DOI:10.1016/j.biopha.2021.112423
摘要
Ferroptosis is a programmed iron-dependent cell death characterized by accumulation of lipid peroxides (LOOH) and redox disequilibrium. Ferroptosis shows unique characteristics in biology, chemistry, and gene levels, compared to other cell death forms. The metabolic disorder of intracellular LOOH catalyzed by iron causes the inactivity of GPX4, disrupts the redox balance, and triggers cell death. Metabolism of amino acid, iron, and lipid, including associated pathways, is considered as a specific hallmark of ferroptosis. Epidemiological studies and animal experiments have shown that ferroptosis plays an important character in the pathophysiology of cardiovascular disease such as atherosclerosis, myocardial infarction (MI), ischemia/reperfusion (I/R), heart failure (HF), cardiac hypertrophy, cardiomyopathy, and abdominal aortic aneurysm (AAA). This review systematically summarized the latest research progress on the mechanisms of ferroptosis. Then we report the contribution of ferroptosis in cardiovascular diseases. Finally, we discuss and analyze the therapeutic approaches targeting for ferroptosis associated with cardiovascular diseases.
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