Ferroptosis: bug or feature?

被引:345
作者
Dixon, Scott J. [1 ]
机构
[1] Stanford Univ, Dept Biol, Stanford, CA 94305 USA
关键词
apoptosis; cysteine; glutathione; necrosis; reactive oxygen species; regulated cell death; GLUTATHIONE-PEROXIDASE; 4; PROGRAMMED CELL-DEATH; POLY(ADP-RIBOSE) POLYMERASE; DNA-DAMAGE; APOPTOSIS; REVEALS; STRESS; METABOLISM; INDUCTION; AUTOPHAGY;
D O I
10.1111/imr.12533
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
071005 [微生物学]; 100108 [医学免疫学];
摘要
Ferroptosis is an iron-dependent, oxidative form of non-apoptotic cell death. This form of cell death does not share morphological, biochemical, or genetic similarities with classic necrosis, necroptosis, parthanatos, or other forms of non-apoptotic cell death. Ferroptosis can be triggered by depleting the cell of the amino acid cysteine, or by inhibiting the phospholipid hydroperoxidase glutathione peroxidase 4 (GPX4). Why certain stimuli trigger ferroptosis instead of another form of cell death, and whether this process could be adaptive in vivo, are two major unanswered questions concerning this process. Emerging evidence and consideration of related non-apoptotic pathways suggest that ferroptosis could be an adaptive process, albeit one regulated and executed in a manner very different from apoptosis and other forms of cell death.
引用
收藏
页码:150 / 157
页数:8
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