Li Yina, Li Mingyang, Feng Shi, Xu Qingxue, Zhang Xu, Xiong Xiaoxing, Gu Lijuan
Central Laboratory; Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China.
Central Laboratory; Department of Neurosurgery, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China.
Neural Regen Res. 2024 Mar;19(3):611-618. doi: 10.4103/1673-5374.380870.
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.
铁死亡是一种非凋亡性程序性细胞死亡形式，其机制主要涉及脂质过氧化物的积累、氨基酸抗氧化系统失衡以及铁代谢紊乱。负责协调外部挑战和内部细胞需求的主要细胞器是内质网，炎症性疾病的进展可引发内质网应激。有证据表明，在许多疾病中，铁死亡可能与内质网应激共享途径或相互作用，并在细胞存活中发挥作用。铁死亡和内质网应激可能在缺血性中风后发生。然而，关于铁死亡和内质网应激与缺血性中风相互作用的报道较少。本综述总结了最近关于铁死亡、内质网应激与缺血性中风之间关系的研究，旨在为开发缺血性中风的治疗方法提供参考。
