中国神经再生研究(英文版) ›› 2024, Vol. 19 ›› Issue (3): 611-618.doi: 10.4103/1673-5374.380870

• 综述:脑损伤修复保护与再生 • 上一篇    下一篇

缺血性脑卒中的铁死亡与内质网应激

  

  • 出版日期:2024-03-15 发布日期:2023-09-02
  • 基金资助:
    国家自然科学基金项目(82071339和82271370)

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).

摘要:

铁死亡是一种非凋亡性的程序性死亡,主要涉及脂质过氧化物的积累、氨基酸抗氧化系统的失衡以及铁代谢紊乱。内质网是一种协调外部应激和内部需求的主要细胞器,炎症性疾病的进展会引发内质网应激。有证据表明,在多种疾病中,铁死亡可能与内质网应激分享相同的信号通路或存在相互作用,协同在细胞存活中发挥作用。缺血性脑卒中后可能发生神经元铁死亡和内质网应激,但是尚且缺乏总结神经元铁死亡和内质网应激与缺血性脑卒中的相互作用。综述总结了近年来铁死亡和内质网应激与缺血性脑卒中关系的最近研究进展,梳理了铁死亡和内质网应激这2种通路之间存在的联系。或可为缺血性脑卒中相关药物的开发提供新的参考。

https://orcid.org/0000-0001-6983-8547 (Xiaoxing Xiong); https://orcid.org/0000-0003-1928-8772 (Lijuan Gu)

关键词: 铁死亡, 缺血性脑卒中, 细胞死亡, 脂质过氧化, 内质网应激

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