Molecular Mechanisms of Ferroptosis and Their Involvement in Acute Kidney Injury

Abstract

Ferroptosis is a novel way of regulating cell death, which occurs in a process that is closely linked to intracellular iron metabolism, lipid metabolism, amino acid metabolism, and multiple signaling pathways. The latest research shows that ferroptosis plays a key role in the pathogenesis of acute kidney injury (AKI). Ferroptosis may be an important target for treating AKI caused by various reasons, such as ischemia-reperfusion injury, rhabdomyolysis syndrome, sepsis, and nephrotoxic drugs. This paper provides a review on the regulatory mechanisms of ferroptosis and its role in AKI, which may help to provide new research ideas for the treatment of AKI and future research.

Keywords:

• ferroptosis
• iron
• lipid peroxidation
• molecular mechanism
• acute kidney injury

Summary

AKI is a common clinical kidney disease that can be caused by various etiologies such as IRI, RM, SA, and nephrotoxic drugs. Ferroptosis, a hot topic of research in recent years, is closely associated with the development of different types of AKI, and a number of small molecule compounds targeting ferroptosis have now demonstrated their ability to prevent and treat AKI. However, the pharmacological mechanisms, toxicity, side effects, and safe doses of the known drugs that inhibit ferroptosis in AKI remain to be further elucidated in future pre-clinical and clinical trials. To sum up, the mechanism of ferroptosis is still developing, but it plays an important role in the occurrence and development of AKI, and the future may be a good potential research direction in the treatment of AKI.

Disclosure

The authors declare no competing interests in this work.

Additional information

Funding

National Natural Science Foundation (81960345, 82260381); Medical Innovation and Development Project of Lanzhou University (lzuyxcx-2022-108).