Neural Regeneration Research ›› 2024, Vol. 19 ›› Issue (3): 611-618.doi: 10.4103/1673-5374.380870

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Ferroptosis and endoplasmic reticulum stress in ischemic stroke

Yina Li1, 2, #, Mingyang Li1, 3, #, Shi Feng1, 3, Qingxue Xu1, 2, Xu Zhang1, 3, Xiaoxing Xiong3, *, Lijuan Gu1, *   

  1. 1Central Laboratory, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China; 2Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China; 3Department of Neurosurgery, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China
  • Online:2024-03-15 Published:2023-09-02
  • Contact: Xiaoxing Xiong, MD, PhD, rm002121@whu.edu.cn; Lijuan Gu, MD, PhD, gulijuan@whu.edu.cn.
  • Supported by:
    This work was supported by the National Natural Science Foundation of China, Nos. 82071339 and 82271370 (both to LG).

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Abstract: 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.

Key words: cell death, endoplasmic reticulum stress, ferroptosis, ischemic stroke, lipid peroxidation