Abstract: 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.

Key words: Acute kidney injury, Ferroptosis, Glutathione peroxidase 4, Ischemia-reperfusion injury, Rhabdomyolysis