- Ischaemic stroke alters local metabolic and inflammatory milieu, driving microglial immunometabolic remodelling and mitochondrial dysfunction that shape inflammation, debris clearance and tissue repair.
- Glycolysis, lactate transport, TCA cycle including succinate, lipid handling and danger sensing interact with mitochondrial redox and quality control to determine microglial function.
- Metabolic effects vary by stroke phase, injury severity and mitochondrial status; resolving divergent findings is essential for evaluating microglial immunometabolism as therapeutic targets.
Transl Stroke Res. 2026 Aug 22;17(5):100. doi: 10.1007/s12975-026-01492-z.
ABSTRACT
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.
PMID:42631879 | DOI:10.1007/s12975-026-01492-z
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