Abstract
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.
Highlights
Cell death is the core of most pathological processes and is an indispensable element of the regulation of normal tissues
The inactivation or absence of glutathione peroxidase 4 (GPX4) causes the accumulation of lipid peroxides, which is regarded as the lethal signal of ferroptotic cell death (Yang et al, 2016; Kagan et al, 2017)
Several pathways are already known to lead to the inhibition of GPX4 and we review them here in association with their corresponding inducers, four small-molecule compounds (Dolma et al, 2003; Yang and Stockwell, 2008; Shimada et al, 2016b; Gaschler et al, 2018a) (Table 1)
Summary
Cell death is the core of most pathological processes and is an indispensable element of the regulation of normal tissues. The inactivation or absence of GPX4 causes the accumulation of lipid peroxides, which is regarded as the lethal signal of ferroptotic cell death (Yang et al, 2016; Kagan et al, 2017). FIN56 induces ferroptosis by two different pathways: promoting the degradation of GPX4 and reducing the abundance of CoQ10 (i.e., an antioxidant in the cell).
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