急性肾损伤(acute kidney injury,AKI)指各种病因引起短时间内肾功能急剧下降而出现的临床综合征，严重者可发展至肾衰竭甚则死亡。铁死亡的发生与谷胱甘肽过氧化物酶4、胱氨酸/谷氨酸反向转运体(cystine/glutamate antiporter,system xc-)、脂质代谢密切相关。铁死亡在缺血再灌注损伤(ischemia reperfusion injury,IRI)、横纹肌溶解(rhabdomyolysis，RM)和叶酸等多种病因所致AKI中均起到重要作用，因而抑制铁死亡在AKI的治疗中具有广阔的前景。本文系统综述了铁死亡参与AKI的作用机制及干预铁死亡的药物研究，探讨其作为治疗靶点的潜在前景。

Acute kidney injury (AKI) is a clinical syndrome characterized by rapid deterioration of kidney function within a short period of time. In severe cases, AKI may lead to kidney failure or even death. Ferroptosis is closely related to glutathione peroxidase 4, cystine-glutamate antiporter (cystine/glutamate antiporter, system Xc-), and lipid metabolism. Ferroptosis plays an important role in ischemia reperfusion injury, rhabdomyolysis, and folic acid and other injuries derived AKI. Therefore, inhibition of ferroptosis may be useful for the treatment of AKI. This article systematically summarizes the mechanism of ferroptosis involved in AKI, the drugs to intervene ferroptosis, and ferroptosis as a potential therapeutic target of AKI.