Mitochondria and ferroptosis
Mitochondria and ferroptosis
复制标题
线粒体和铁死亡
DOI：
10.1016/j.cophys.2022.100483
复制
发表时间：
2022-02-02
影响因子：
2.5
通讯作者：
Javadov, Sabzali
中科院分区：
文献类型：
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作者：
Javadov, Sabzali
铁死亡是一种受调控的铁依赖性细胞死亡机制，伴随着细胞中过氧化磷脂，特别是磷脂酰乙醇胺的积累。它的发生是由于氧化磷脂的产生和消除之间的不平衡，以响应铁致刺激。最近越来越多的研究表明，铁下垂参与了各种人类疾病的发病机制，导致器官/组织异常。由于线粒体在ATP合成、ROS产生、铁稳态和氧化还原状态中起着核心作用，因此人们提出线粒体介导铁致凋亡信号通路。然而，线粒体在铁下垂中潜在作用的确切机制仍未揭示。这篇综述总结和讨论了线粒体对铁亡细胞死亡的贡献，并强调了未来的研究方向，阐明线粒体作为一个有希望的靶点，通过阻断铁亡来防止细胞死亡。
Ferroptosis is a regulated iron-dependent cell death mechanism accompanied by the accumulation of peroxidized phospholipids, particularly phosphatidylethanolamine, in the cell. It occurs due to the disbalance between production and elimination of oxidized phospholipids in response to ferroptotic stimuli. A growing body of recent studies indicates that ferroptosis is involved in the pathogenesis of various human diseases leading to organ/tissue abnormalities. Because of their central role in ATP synthesis, ROS production, iron homeostasis, and redox status, mitochondria have been proposed to mediate ferroptotic signaling pathways. However, precise mechanisms underlying the potential role of mitochondria in ferroptosis remain unrevealed. This review summarizes and discusses previous studies on the contribution of mitochondria to ferroptotic cell death and highlights future directions elucidating the mitochondria as a promising target to prevent cell death through blocking ferroptosis.