中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2026, Vol. 21 ›› Issue (6): 2315-2329.doi: 10.4103/NRR.NRR-D-24-00301

• 综述:脑损伤修复保护与再生 • 上一篇    下一篇

缺血性脑卒中的细胞凋亡：关注脂质代谢

  

  • 出版日期:2026-06-15 发布日期:2025-09-18

Cell apoptosis in ischemic stroke: Focus on lipid metabolism

Rong Sun1, 2, #, Wenren Yang3, #, Yuting Zhao1, 2, Fumei Zhang1, 2, Genping Wu1, 2, Aiping Wang4, *, Ying Tian1, 2, *   

  1. 1 Institute of Clinical Research, Department of Clinical Laboratory, Affiliated Nanhua Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan Province, China;  2 Department of Biochemistry and Molecular Biology, Hengyang Medical School, University of South China, Hengyang, Hunan Province, China;  3 Department of Trauma Center, Affiliated Nanhua Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan Province, China;  4 Department of Physiology, Institute of Neuroscience Research, Hengyang Medical School, University of South China, Hengyang, Hunan Province, China
  • Online:2026-06-15 Published:2025-09-18
  • Contact: Aiping Wang, waiping2011@163.com or waiping2011@usc.edu.cn; Ying Tian, uscty@163.com.
  • Supported by:
    This work was supported by the National Natural Science Foundation of China, Nos. 31871169 (to YT), 32471179 (to AW); the Natural Science Foundation of Hunan Province, No. 2021JJ30601 (to AW); Key Program of Education Department of Hunan Province, No. 21A0274 (to AW).

PDF

16

摘要：

研究认为，动脉粥样硬化是缺血性脑卒中的主要原因，而血脂水平异常是动脉粥样硬化的重要诱因。脂质代谢紊乱导致的缺血性脑卒中涉及多种细胞凋亡机制。此外，各种脂质与神经细胞凋亡有着密切的因果关系。然而，目前的科学研究还缺乏对脂质代谢导致缺血性脑卒中细胞凋亡的总结。以往的研究仅关注脂质代谢或细胞凋亡在缺血性脑卒中中的作用。此综述总结了目前有关缺血性脑卒中中脂质的研究。它讨论了脂质代谢在缺血性脑卒中加速细胞凋亡的作用和机制，还通过关注脂质代谢概述了治疗缺血性脑卒中的新药物和新进展，并为缺血性脑卒中的治疗和预防提供新的思路和策略。

https://orcid.org/0000-0003-3392-0543 (Aiping Wang); https://orcid.org/0000-0002-7748-1610 (Ying Tian)

关键词: 二十二碳六烯酸, 二十碳五烯酸, 高密度脂蛋白, 低密度脂蛋白, 活性氧, 短链脂肪酸, 甘油三酯, 肿瘤坏死因子

Abstract: Ischemic stroke is a severe neurological disease with high global mortality and disability rates. Atherosclerosis has been identified as the primary cause of ischemic stroke, while abnormal lipid levels are significant contributors to the development of this condition. Multiple pro-apoptotic mechanisms are involved in ischemic stroke caused by lipid metabolism disorders, while various lipids have a strong causal relationship with neuronal apoptosis. However, studies to date have focused on the individual roles of lipid metabolism and apoptosis in ischemic stroke, and an overview of how impaired lipid metabolism leads to apoptosis in ischemic stroke is still lacking in the literature. In this review, we summarize current research on lipids in ischemic stroke. We discuss the role of lipid metabolism in accelerating apoptosis in ischemic stroke as well as the associated mechanisms. Additionally, we highlight advances in drug development and the treatment of stroke, focusing on lipid metabolism. The purpose is to provide novel ideas and strategies for the treatment and prevention of ischemic stroke.

Key words: docosahexaenoic acid, eicosapentaenoic acid, high-density lipoprotein, low-density lipoprotein, reactive oxygen species, short-chain fatty acids, triglycerides, tumor necrosis factor