REVIEW article

Front. Cell Dev. Biol.

Sec. Cellular Biochemistry

Volume 13 - 2025 | doi: 10.3389/fcell.2025.1614156

This article is part of the Research TopicInnovative Therapeutic Strategies for Chronic Kidney Disease: From Molecular Mechanisms to Clinical PracticeView all 4 articles

Research progress of ferroptosis in acute kidney injury

Provisionally accepted
Lin ZhangLin Zhang1Feng LuoFeng Luo2*Nan YuanNan Yuan1Jiaming YinJiaming Yin1Bing ShenBing Shen1Yalin ChaiYalin Chai1Lijie SunLijie Sun1Xuan WangXuan Wang1Le YinLe Yin1Congjuan LuoCongjuan Luo1*
  • 1Department of Nephrology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong Province, China
  • 2Department of cardiology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong Province, China

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Acute kidney injury (AKI) is a life-threatening condition characterized by a rapid decline in kidney function caused by various underlying factors. Despite advancements in medical science, effective treatments for AKI remain limited, highlighting the necessity for novel therapeutic strategies. Ferroptosis, an iron-dependent regulated cell death characterized by lipid peroxidation, has been recently linked to AKI development. Studies indicate that ferroptosis plays a role in multiple AKI types, such as those caused by ischemia-reperfusion, sepsis, nephrotoxic agents, and rhabdomyolysis. In these conditions, ferroptosis markers are elevated in renal tubular epithelial cells, and inhibiting ferroptosis has been shown to reduce kidney injury. However, the precise regulatory mechanisms of ferroptosis in AKI remain unclear. This review summarizes current understanding of ferroptosis, including its definition, molecular regulation, involvement in various AKI types, and potential therapeutic targets. By elucidating these aspects, we hope to provide a foundation for future research and the development of effective interventions for AKI.

Keywords: Acute Kidney Injury, ferroptosis, Lipid Peroxidation, mechanisms, therapeutic targets

Received: 18 Apr 2025; Accepted: 17 Jun 2025.

Copyright: © 2025 Zhang, Luo, Yuan, Yin, Shen, Chai, Sun, Wang, Yin and Luo. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence:
Feng Luo, Department of cardiology, The Affiliated Hospital of Qingdao University, Qingdao, 266000, Shandong Province, China
Congjuan Luo, Department of Nephrology, The Affiliated Hospital of Qingdao University, Qingdao, 266000, Shandong Province, China

Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

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