文献类型：期刊文献

英文题名：Microglial Immunometabolic Remodeling After Ischemic Stroke: The Interplay Between Mitochondrial Stress and the Ischemic Microenvironment

作者：Liu, Cui[1];Liu, Qiang[1];Jing, Weiyao[2];Liu, Limei[3];Wei, Long[1];Li, Xing[1];Du, Xiaozheng[1]

第一作者：柳春

通信作者：Du, XZ[1]

机构：[1]Gansu Univ Tradit Chinese Med, Sch Acupuncture & Tuina, Lanzhou 730000, Peoples R China;[2]Weifang Hosp Tradt Chinese Med, Acupuncture Dept, Weifang 261041, Peoples R China;[3]Gansu Univ Tradit Chinese Med, Affiliated Hosp, Zhengs Acupuncture Dept, Lanzhou 730030, Peoples R China

第一机构：甘肃中医药大学

通信机构：[1]corresponding author), Gansu Univ Tradit Chinese Med, Sch Acupuncture & Tuina, Lanzhou 730000, Peoples R China.|[10735]甘肃中医药大学;

年份：2026

卷号：17

期号：5

外文期刊名：TRANSLATIONAL STROKE RESEARCH

收录：;Scopus(收录号：2-s2.0-105047920751);WOS:【SCI-EXPANDED(收录号:WOS:001855218200002)】；

基金：National Natural Science Foundation of China (No. 82460965); Gansu Province Administration of Traditional Chinese Medicine Project (GZKZ-2024-35).

语种：英文

外文关键词：Microglia; Metabolic regulation; Mitochondria; Ischemic stroke

摘要：Following ischemic stroke, marked alterations in the local metabolic and inflammatory milieu of the brain drive immunometabolic remodeling and mitochondrial dysfunction in microglia, thereby shaping inflammation, damage clearance, and tissue repair. Existing studies have largely focused on individual metabolic pathways, leaving the relationships among the ischemic microenvironment, mitochondrial responses, and microglial functional changes incompletely understood. Available evidence indicates that the effects of these metabolic alterations vary with stroke phase, local injury severity, and mitochondrial status. This review summarizes current evidence on glycolysis and lactate transport, the tricarboxylic acid cycle and succinate signaling, lipid handling, and danger-signal sensing, with particular emphasis on their relationships with mitochondrial redox homeostasis and quality control. We also critically evaluate divergent findings across studies. By examining the interaction between the ischemic microenvironment and mitochondrial responses, this review aims to clarify the metabolic basis of microglial functional changes and to inform the assessment of potential therapeutic targets in microglial immunometabolism.