铁死亡受基因调控，参与缺血再灌注损伤、脑卒中、肿瘤等疾病的生理和病理过程，致病机制尚未明确。已知调控p53基因可诱导内皮细胞和肿瘤细胞铁死亡。而抑制铁死亡使GPX4正常发挥作用，阻断细胞膜上脂质氧化，减少活性氧自由基（ROS）积累，保护正常细胞。鉴于铁死亡的多反应性，可能有助于杀死癌细胞，可能会损伤正常细胞，所以调节性铁死亡敏感相关基因及触发机制亟待阐明。本文主要综述目前已知的GPX4、FSP1、SLC7A11、P53等调节性铁死亡敏感相关基因功能机制，以期为铁死亡研究深度剖析及重大疾病药物靶向选择提供参考。

Ferroptosis is regulated by genes and participates in the physiological and pathological processes of ischemia-reperfusion injury， stroke， tumor and other diseases. The pathogenic mechanism is not yet clear. It is known that regulating p53 gene can induce ferroptosis of endothelial cells and tumor cells. Inhibiting ferroptosis enables GPX4 to function normally， blocking lipid oxidation on cell membranes， reducing the accumulation of reactive oxygen species （ROS）， and protecting normal cells. In view of the polyreactivity of ferroptosis， it may help kill cancer cells and may damage normal cells. Therefore， genes related to regulatory ferroptosis sensitivity and the trigger mechanism need to be elucidated urgently. This article mainly reviews the known functional mechanisms of regulatory ferroptosis sensitive genes such as GPX4， FSP1， SLC7A11， P53， et al，in order to provide a reference for the in-depth analysis of ferroptosis research and the selection of drugs for major diseases.

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国家自然科学基金资助项目（81960663）