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Published on: June 20, 2025
Microglial Immunometabolic Remodeling After Ischemic Stroke: The Interplay Between Mitochondrial Stress and the
Cui Liu1, Qiang Liu1, Weiyao Jing2
1School of Acupuncture and Tuina, Gansu University of Traditional Chine se Medicine, Lanzhou, 730000, China.
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.
Insights
Ischemic stroke alters brain metabolism and microglia function. Understanding these immunometabolic changes and mitochondrial responses is key to developing new stroke therapies.
Area of Science:
- Neuroscience
- Immunology
- Metabolism
Background:
- Ischemic stroke triggers significant changes in the brain's metabolic and inflammatory environment.
- These changes impact microglial (brain immune cell) function, leading to immunometabolic remodeling and mitochondrial dysfunction.
- Current research often focuses on single metabolic pathways, leaving the interplay between the ischemic environment, mitochondrial activity, and microglial responses unclear.
Purpose of the Study:
- To review and synthesize current evidence on microglial immunometabolism following ischemic stroke.
- To elucidate the relationships between the ischemic microenvironment, mitochondrial function, and microglial functional states.
- To identify potential therapeutic targets for stroke by clarifying the metabolic basis of microglial responses.
Main Methods:
- Literature review of existing studies on microglial metabolism in ischemic stroke.
- Focus on key metabolic pathways: glycolysis, lactate transport, TCA cycle, succinate signaling, lipid handling, and danger-signal sensing.
- Emphasis on the connection between these pathways, mitochondrial redox homeostasis, and quality control.
Main Results:
- Metabolic alterations in stroke vary based on stroke phase, injury severity, and mitochondrial status.
- Specific metabolic pathways (glycolysis, lipid handling, etc.) critically influence microglial inflammation, debris clearance, and repair.
- Mitochondrial redox balance and quality control are central to mediating these metabolic effects.
Conclusions:
- The interplay between the ischemic microenvironment and mitochondrial responses dictates microglial functional outcomes.
- Clarifying microglial immunometabolism is essential for understanding stroke pathology.
- This review provides a foundation for developing targeted immunometabolic therapies for stroke.
