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The main molecular mechanisms of ferroptosis and its role in chronic kidney disease

The term ferroptosis, coined in 2012, has been widely applied in various disease research fields. Ferroptosis is a newly regulated form of cell death distinct from apoptosis, necrosis, and autophagy, the mechanisms of which have been extensively studied. Chronic kidney disease, characterized by rena...

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Published in:Cellular signalling 2024-09, Vol.121, p.111256, Article 111256
Main Authors: Wang, Fulin, Huang, Xuesong, Wang, Shaokun, Wu, Dawei, Zhang, Meiying, Wei, Wei
Format: Article
Language:English
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Summary:The term ferroptosis, coined in 2012, has been widely applied in various disease research fields. Ferroptosis is a newly regulated form of cell death distinct from apoptosis, necrosis, and autophagy, the mechanisms of which have been extensively studied. Chronic kidney disease, characterized by renal dysfunction, is a common disease severely affecting human health, with its occurrence and development influenced by multiple factors and leading to dysfunction in multiple systems. It often lacks obvious clinical symptoms in the early stages, and thus, diagnosis is typically made in the later stages, complicating treatment. While research on ferroptosis and acute kidney injury has made continuous progress, studies on the association between ferroptosis and chronic kidney disease remain limited. This review aims to summarize chronic kidney disease, investigate the mechanism and regulation of ferroptosis, and attempt to elucidate the role of ferroptosis in the occurrence and development of chronic kidney disease. •Ferroptosis is a new type of regulated cell death different from apoptosis, necrosis and autophagy.•CKD is a common disease characterized by renal dysfunction, which seriously affects human life and health.•Ferroptosis is closely related to iron overload and lipid peroxidation.•Ferroptosis plays an important role in the occurrence and development of CKD.
ISSN:0898-6568
1873-3913
1873-3913
DOI:10.1016/j.cellsig.2024.111256