Ferroptosis and endoplasmic reticulum stress in ischemic stroke

Ferroptosis is a form of non-apoptotic programmed cell death, and its mechanisms mainly involve the accumulation of lipid peroxides, imbalance in the amino acid antioxidant system, and disordered iron metabolism. The primary organelle responsible for coordinating external challenges and internal cel...

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Published inNeural regeneration research Vol. 19; no. 3; pp. 611 - 618
Main Authors Li, Yina, Li, Mingyang, Feng, Shi, Xu, Qingxue, Zhang, Xu, Xiong, Xiaoxing, Gu, Lijuan
Format Journal Article
LanguageEnglish
Published Mumbai Wolters Kluwer India Pvt. Ltd 01.03.2024
Medknow Publications & Media Pvt. Ltd
Department of Anesthesiology,Renmin Hospital of Wuhan University,Wuhan,Hubei Province,China%Central Laboratory,Renmin Hospital of Wuhan University,Wuhan,Hubei Province,China
Department of Neurosurgery,Renmin Hospital of Wuhan University,Wuhan,Hubei Province,China%Department of Neurosurgery,Renmin Hospital of Wuhan University,Wuhan,Hubei Province,China%Central Laboratory,Renmin Hospital of Wuhan University,Wuhan,Hubei Province,China
Central Laboratory,Renmin Hospital of Wuhan University,Wuhan,Hubei Province,China
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Summary:Ferroptosis is a form of non-apoptotic programmed cell death, and its mechanisms mainly involve the accumulation of lipid peroxides, imbalance in the amino acid antioxidant system, and disordered iron metabolism. The primary organelle responsible for coordinating external challenges and internal cell demands is the endoplasmic reticulum, and the progression of inflammatory diseases can trigger endoplasmic reticulum stress. Evidence has suggested that ferroptosis may share pathways or interact with endoplasmic reticulum stress in many diseases and plays a role in cell survival. Ferroptosis and endoplasmic reticulum stress may occur after ischemic stroke. However, there are few reports on the interactions of ferroptosis and endoplasmic reticulum stress with ischemic stroke. This review summarized the recent research on the relationships between ferroptosis and endoplasmic reticulum stress and ischemic stroke, aiming to provide a reference for developing treatments for ischemic stroke.
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Author contributions: Manuscript design: LG, XX; literature review: ML; figure preparation: SF; initial draft: YL; literature collection and table figure preparation: QX, XZ. All authors have read and approved the final version of the manuscript.
Both authors contributed equally to this work.
ISSN:1673-5374
1876-7958
DOI:10.4103/1673-5374.380870