GPX4
脂质过氧化
疾病
程序性细胞死亡
医学
药理学
氧化应激
心肌梗塞
化学
癌症研究
谷胱甘肽过氧化物酶
细胞凋亡
生物化学
内科学
超氧化物歧化酶
作者
Zahra Shaghaghi,Shokouh Motieian,Maryam Alvandi,Amirhossein Yazdi,Bahareh Asadzadeh,Soghra Farzipour,Sahar Abbasi
出处
期刊:Mini-reviews in Medicinal Chemistry
[Bentham Science]
日期:2022-09-01
卷期号:22 (17): 2271-2286
被引量:13
标识
DOI:10.2174/1389557522666220218123404
摘要
Ferroptosis is a novel form of programmed cell death that occurs due to an increase in iron levels. Ferroptosis is implicated in a number of cardiovascular diseases, including myocardial infarction (MI), reperfusion damage, and heart failure (HF). As cardiomyocyte depletion is the leading cause of patient morbidity and mortality, it is critical to thoroughly comprehend the regulatory mechanisms of ferroptosis activation. In fact, inhibiting cardiac ferroptosis can be a useful therapeutic method for cardiovascular disorders. The iron, lipid, amino acid, and glutathione metabolisms strictly govern the beginning and execution of ferroptosis. Therefore, ferroptosis can be inhibited by iron chelators, free radical-trapping antioxidants, GPX4 (Glutathione Peroxidase 4) activators, and lipid peroxidation (LPO) inhibitors. However, the search for new molecular targets for ferroptosis is becoming increasingly important in cardiovascular disease research. In this review, we address the importance of ferroptosis in various cardiovascular illnesses, provide an update on current information regarding the molecular mechanisms that drive ferroptosis, and discuss the role of ferroptosis inhibitors in cardiovascular disease.
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