Javadov Sabzali
Department of Physiology, University of Puerto Rico School of Medicine, San Juan, PR 00936-5067, USA.
Curr Opin Physiol. 2022 Feb;25. doi: 10.1016/j.cophys.2022.100483. Epub 2022 Jan 22.
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. Due to 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.
铁死亡是一种受调控的铁依赖性细胞死亡机制，伴随着过氧化磷脂尤其是磷脂酰乙醇胺在细胞内的积累。它是由于在铁死亡刺激下氧化磷脂的产生和消除失衡而发生的。最近越来越多的研究表明，铁死亡参与了导致器官/组织异常的各种人类疾病的发病机制。由于线粒体在ATP合成、活性氧生成、铁稳态和氧化还原状态中发挥核心作用，有人提出线粒体可介导铁死亡信号通路。然而，线粒体在铁死亡中潜在作用的精确机制仍未明确。本综述总结并讨论了先前关于线粒体对铁死亡细胞死亡贡献的研究，并强调了未来的研究方向，即阐明线粒体作为通过阻断铁死亡来预防细胞死亡的一个有前景的靶点。
