The mechanisms of ferroptosis and its role in atherosclerosis

GPX4 磷脂过氧化氢谷胱甘肽过氧化物酶 脂质过氧化 程序性细胞死亡 活性氧 氧化应激 细胞生物学 细胞凋亡 谷胱甘肽 化学 癌症研究 生物 药理学 生物化学 谷胱甘肽过氧化物酶 超氧化物歧化酶
作者
Xi Xu,Xiaodan Xu,Mengqing Ma,Yin Liang,Yang-Bo Cai,Zi-Xian Zhu,Tao Xu,Lin Zhu,Kun Ren
出处
期刊:Biomedicine & Pharmacotherapy [Elsevier BV]
卷期号:171: 116112-116112 被引量:41
标识
DOI:10.1016/j.biopha.2023.116112
摘要

Ferroptosis is a newly identified form of non-apoptotic programmed cell death, characterized by the iron-dependent accumulation of lethal lipid reactive oxygen species (ROS) and peroxidation of membrane polyunsaturated fatty acid phospholipids (PUFA-PLs). Ferroptosis is unique among other cell death modalities in many aspects. It is initiated by excessive oxidative damage due to iron overload and lipid peroxidation and compromised antioxidant defense systems, including the system Xc-/ glutathione (GSH)/glutathione peroxidase 4 (GPX4) pathway and the GPX4-independent pathways. In the past ten years, ferroptosis was reported to play a critical role in the pathogenesis of various cardiovascular diseases, e.g., atherosclerosis (AS), arrhythmia, heart failure, diabetic cardiomyopathy, and myocardial ischemia-reperfusion injury. Studies have identified dysfunctional iron metabolism and abnormal expression profiles of ferroptosis-related factors, including iron, GSH, GPX4, ferroportin (FPN), and SLC7A11 (xCT), as critical indicators for atherogenesis. Moreover, ferroptosis in plaque cells, i.e., vascular endothelial cell (VEC), macrophage, and vascular smooth muscle cell (VSMC), positively correlate with atherosclerotic plaque development. Many macromolecules, drugs, Chinese herbs, and food extracts can inhibit the atherogenic process by suppressing the ferroptosis of plaque cells. In contrast, some ferroptosis inducers have significant pro-atherogenic effects. However, the mechanisms through which ferroptosis affects the progression of AS still need to be well-known. This review summarizes the molecular mechanisms of ferroptosis and their emerging role in AS, aimed at providing novel, promising druggable targets for anti-AS therapy.
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