GPX4
疾病
医学
心力衰竭
活性氧
程序性细胞死亡
氧化应激
脂质过氧化
缺血
死因
机制(生物学)
病理生理学
谷胱甘肽过氧化物酶
心脏病学
内科学
生物
细胞生物学
细胞凋亡
超氧化物歧化酶
生物化学
哲学
认识论
作者
Anna Fratta Pasini,Chiara Stranieri,Fabiana Busti,Edoardo Giuseppe Di Leo,Domenico Girelli,Luciano Cominacini
出处
期刊:Cells
[MDPI AG]
日期:2023-03-10
卷期号:12 (6): 867-867
标识
DOI:10.3390/cells12060867
摘要
Cardiovascular diseases (CVDs) are the principal cause of disease burden and death worldwide. Ferroptosis is a new form of regulated cell death mainly characterized by altered iron metabolism, increased polyunsaturated fatty acid peroxidation by reactive oxygen species, depletion of glutathione and inactivation of glutathione peroxidase 4. Recently, a series of studies have indicated that ferroptosis is involved in the death of cardiac and vascular cells and has a key impact on the mechanisms leading to CVDs such as ischemic heart disease, ischemia/reperfusion injury, cardiomyopathies, and heart failure. In this article, we reviewed the molecular mechanism of ferroptosis and the current understanding of the pathophysiological role of ferroptosis in ischemic heart disease and in some cardiomyopathies. Moreover, the comprehension of the machinery governing ferroptosis in vascular cells and cardiomyocytes may provide new insights into preventive and therapeutic strategies in CVDs.
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