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Ferroptosis: bug or feature?

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IMMUNOLOGICAL REVIEWS
卷 277, 期 1, 页码 150-157

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WILEY
DOI: 10.1111/imr.12533

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apoptosis; cysteine; glutathione; necrosis; reactive oxygen species; regulated cell death

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  1. National Cancer Institute [4R00CA166517-03]

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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.

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