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铁死亡是近年来新发现的一种调节性的细胞死亡方式，主要是由于谷胱甘肽过氧化物酶(glutathione peroxidase 4，GPX4)缺乏、铁代谢异常、脂质过氧化等原因导致的细胞死亡。目前认为铁代谢和活性氧代谢是铁死亡的中心环节。铁死亡涉及多种生理和病理过程，包括癌细胞死亡、神经毒性、缺血再灌注损伤和T细胞免疫等。研究表明，在多种肾病的发生发展过程中可出现不同程度的铁过载及脂质过氧化等铁死亡特征。铁死亡可以通过调节细胞内铁离子水平及脂质过氧化程度，影响肾脏疾病的进程。因此，有效调控铁死亡有望成为治疗肾脏疾病的重要策略。该文对铁死亡的调控机制及其在肾脏疾病中的研究进展进行综述，为肾脏疾病的治疗提供新的理论和思路。“,”Ferroptosis is a newly discovered regulatory mode of cell death, which is caused by glutathione peroxidase 4 deficiency, abnormal iron metabolism and lipid peroxidation.At present, it is considered that iron metabolism and active oxygen metabolism are the central link of ferroptosis.Ferroptosis involves a variety of physiological and pathological processes, including cancer cell death, neurotoxicity, ischemia-reperfusion injury, and T-cell immunity.Studies have shown that ferroptosis characteristics such as iron overload and lipid peroxidation may occur in different degrees during the development of a variety of nephropathy.Ferroptosis can affect the progression of renal disease by regulating the level of intracellular iron ions and lipid peroxidation.Therefore, effective regulation of ferroptosis is expected to be an important strategy in the treatment of renal diseases.In this paper, the regulation mechanism of ferroptosis and its research progress in kidney disease are reviewed to provide new theories and ideas for the treatment of renal disease.