GPX4
程序性细胞死亡
脂质过氧化
细胞生物学
磷脂过氧化氢谷胱甘肽过氧化物酶
机制(生物学)
细胞
化学
过氧化物酶
谷胱甘肽
氧化应激
生物化学
细胞凋亡
生物
谷胱甘肽过氧化物酶
酶
哲学
认识论
作者
Pengxu Lei,Tao Bai,Yuling Sun
标识
DOI:10.3389/fphys.2019.00139
摘要
Ferroptosis is a newly identified form of nonapoptotic regulated cell death (RCD) characterized by iron-dependent accumulation of lipid peroxides. It is morphologically and biochemically different from known types of cell death. Ferroptosis plays a vital role in the treatment of tumors, renal failure, and ischemia reperfusion injury (IRI). Inhibition of glutathione peroxidase 4 (GPX4), starvation of cysteine, and peroxidation of arachidonoyl (AA) trigger ferroptosis in the cells. Iron chelators, lipophilic antioxidants, and specific inhibitor prevent ferroptosis. Although massive researches have demonstrated the importance of ferroptosis in human, its mechanism is not really clear. In this review, we distanced ourselves from this confusion by dividing the mechanisms of ferroptosis into two aspects: processes that facilitate the formation of lipid peroxides and processes that suppress the reduction of lipid peroxides. At the same time, we summarize the relations between ferroptosis and several types of cell death.
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