国际医药卫生导报 ›› 2025, Vol. 31 ›› Issue (22): 3698-3703.DOI: 10.3760/cma.j.cn441417-20250515-22001

• 脑卒中专题 •    下一篇

铁死亡在缺血性脑卒中的作用机制及研究进展

刘晏民  汪临华  李婷婷  宋盈娴  王美玲   

  1. 滨州医学院附属医院神经内科,滨州 256603
  • 收稿日期:2025-05-15 出版日期:2025-11-01 发布日期:2025-11-19
  • 通讯作者: 王美玲,Email:wmc_111@126.com
  • 基金资助:
    山东省医药卫生科技发展计划(2018WS539)

The mechanism and research progress of ferroptosis in ischemic stroke

Liu Yanmin, Wang Linhua, Li Tingting, Song Yingxian, Wang Meiling   

  1. Department of Neurology, Binzhou Medical University Hospital, Binzhou 256603, China
  • Received:2025-05-15 Online:2025-11-01 Published:2025-11-19
  • Contact: Wang Meiling, Email: wmc_111@126.com
  • Supported by:
    Shandong Provincial Medical and Health Science and Technology Development Plan(2018WS539)

摘要: 缺血性脑卒中(IS)作为一种全球高发病率和高病死率的脑血管疾病,一直以来都缺乏有效的治疗手段,而铁死亡作为一种铁依赖性的细胞死亡方式,随着研究进展,其在IS病理过程中的作用被逐渐阐明。铁死亡不仅可以通过铁过载、氧化还原失调和脂质过氧化加剧神经损伤,还可以通过相关信号通路进行调控。目前,针对铁死亡作用机制的抑制剂已被证明能够减轻IS后的神经损伤并改善预后。本文综述了铁死亡在IS中的发病机制、相关信号通路、相关抑制剂的潜在治疗效果以及与其他细胞死亡的交叉作用,旨在为未来临床研究和治疗策略提供新的思路和方向。

关键词: 缺血性脑卒中, 铁死亡, 铁过载, 脂质过氧化, 抑制剂, 进展

Abstract: Ischemic stroke (IS), a cerebrovascular disease with high global morbidity and mortality, has long lacked effective therapeutic approaches. Ferroptosis, an iron-dependent form of cell death, has been progressively elucidated in IS pathogenesis through ongoing research. Ferroptosis not only exacerbates neurological damage through iron overload, redox imbalance, and lipid peroxidation, but is also regulated by associated signaling pathways. Currently, inhibitors targeting ferroptosis mechanisms have been demonstrated to mitigate post-IS neuronal damage and improve prognosis. This review systematically summarizes the pathogenic role of ferroptosis in IS, analyzes its associated signaling pathways, the potential therapeutic effects of associated inhibitors, and its interplay with other forms of cell death, aiming to provide novel insights and directions for future clinical research and therapeutic strategies.

Key words: Ischemic stroke, Ferroptosis, Iron overload, Lipid peroxidation, Inhibitor, Progress