{"title":"Regulatory mechanism of ferroptosis in acute kidney injury and potential therapeutic strategies","authors":"Wendi Zhong , Zihuang Xie , Siqi Wei , Tian Zhong , Tao Jiang","doi":"10.1016/j.lfs.2025.123828","DOIUrl":null,"url":null,"abstract":"<div><div>Ferroptosis is a type of iron-dependent programmed cell death distinguished by increased oxidative stress and the pathological accumulation of lipid peroxides within the cell membrane. Emerging evidence suggests a strong link between ferroptosis and both the occurrence and progression of acute kidney injury (AKI). However, many outstanding issues remain to be solved in the development of drugs that target ferroptosis. Therefore, it is imperative to present a comprehensive overview of the most recent advancements in the field of ferroptosis. In this review, we systematically summarize the predisposing factors and defense mechanisms of ferroptosis in AKI. Moreover, we focused on the role of specific regulators related to ferroptosis, including STING, CX3CL1, FXR, and CD36, in AKI. These regulatory factors may be potential targets for treating AKI in the future. Additionally, potential strategies for preventing AKI by targeting ferroptosis were also highlighted in this study. Numerous studies have demonstrated that targeting ferroptosis to alleviate inflammation and renal fibrosis, modulate metabolic reprogramming, and regulate reactive oxygen species may represent an effective strategy for mitigating the progression of AKI. These findings offer novel potential targets and therapeutic strategies for managing AKI through ferroptosis.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"378 ","pages":"Article 123828"},"PeriodicalIF":5.2000,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Life sciences","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0024320525004631","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}
引用次数: 0
Abstract
Ferroptosis is a type of iron-dependent programmed cell death distinguished by increased oxidative stress and the pathological accumulation of lipid peroxides within the cell membrane. Emerging evidence suggests a strong link between ferroptosis and both the occurrence and progression of acute kidney injury (AKI). However, many outstanding issues remain to be solved in the development of drugs that target ferroptosis. Therefore, it is imperative to present a comprehensive overview of the most recent advancements in the field of ferroptosis. In this review, we systematically summarize the predisposing factors and defense mechanisms of ferroptosis in AKI. Moreover, we focused on the role of specific regulators related to ferroptosis, including STING, CX3CL1, FXR, and CD36, in AKI. These regulatory factors may be potential targets for treating AKI in the future. Additionally, potential strategies for preventing AKI by targeting ferroptosis were also highlighted in this study. Numerous studies have demonstrated that targeting ferroptosis to alleviate inflammation and renal fibrosis, modulate metabolic reprogramming, and regulate reactive oxygen species may represent an effective strategy for mitigating the progression of AKI. These findings offer novel potential targets and therapeutic strategies for managing AKI through ferroptosis.
期刊介绍:
Life Sciences is an international journal publishing articles that emphasize the molecular, cellular, and functional basis of therapy. The journal emphasizes the understanding of mechanism that is relevant to all aspects of human disease and translation to patients. All articles are rigorously reviewed.
The Journal favors publication of full-length papers where modern scientific technologies are used to explain molecular, cellular and physiological mechanisms. Articles that merely report observations are rarely accepted. Recommendations from the Declaration of Helsinki or NIH guidelines for care and use of laboratory animals must be adhered to. Articles should be written at a level accessible to readers who are non-specialists in the topic of the article themselves, but who are interested in the research. The Journal welcomes reviews on topics of wide interest to investigators in the life sciences. We particularly encourage submission of brief, focused reviews containing high-quality artwork and require the use of mechanistic summary diagrams.