GPX4
程序性细胞死亡
磷脂过氧化氢谷胱甘肽过氧化物酶
活性氧
细胞生物学
过氧化脂质
癌症研究
细胞内
化学
细胞
脂质过氧化
医学
MAPK/ERK通路
癌症
生物
信号转导
计算生物学
癌细胞
机制(生物学)
生物化学
细胞凋亡
坏死性下垂
氧化应激
过氧化氢酶
谷胱甘肽过氧化物酶
哲学
认识论
作者
B. Mahalakshmi,Bharath Kumar Velmurugan
标识
DOI:10.1016/j.cbi.2019.108930
摘要
Ferroptosis is recently identified form of regulated cell death which differs from previously identified cell death in a way that it is driven by iron-dependent lipid peroxide accumulation. Morphologically, cell volume shrinkage and increased mitochondrial membrane density are main features which characterize this form of cell death. Molecular mechanism of ferroptosis induction involved suppression of the phospholipid glutathione peroxidase 4 (GPX4) and further intracellular accumulation of lipid reactive oxygen species (ROS), a process in which iron is involved; either via inhibition of system Xc- (cystine/glutamate antiporter) or direct inhibition of GPX4. Several other pathways like RAS/MAPK and NRF2 are found to be involved in ferroptosis regulation. However, the precise mechanism of ferroptosis induction is not revealed till date. Like other regulated cell deaths, ferroptosis plays important role in tumor suppression and progression as revealed by several scientific reports. This review summarizes basic information about discovery of this novel cell death mechanism including molecular mechanism of its induction and further explains the roles of ferroptosis in human cancers.
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