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Updated: Sep 10, 2025
Isolation and Flow Cytometric Assessment of Neuroimmune Interactions in a Mini-Stroke Murine Model
Published on: June 20, 2025
Role and Mechanism of Microglia in White Matter Injury Recovery in Ischemic Stroke
Yi-Sha Guo1, Yunlin Shang1, Jiajia Yao1
1Department of Physical Therapy, Affiliated Yangzhi Rehabilitation Hospital of Tongji University, Shanghai Yangzhi Rehabilitation Hospital, Shanghai, China.
Background:
Ischemic stroke frequently leads to white matter injury (WMI), significantly impairing neurological function and recovery. Microglia, the central nervous system's resident immune cells, play a dual role in poststroke pathology and repair. Their diverse activation states and interactions with other glial cells influence demyelination, remyelination, and overall WMI outcomes. To systematically review and synthesize the current evidence regarding the temporal and functional dynamics of microglia in ischemic stroke, with a focus on their roles in white matter damage and recovery.
Methods:
A comprehensive literature search was conducted using PubMed, Web of Science, and Scopus databases (through December 2024) with keywords including "ischemic stroke," "white matter injury," "microglia," "myelin," and "oligodendrocytes." Studies involving mechanistic insights into microglial polarization, myelin repair, and associated molecular pathways were prioritized. Both preclinical and clinical studies were reviewed.
Results:
Microglia exhibit distinct activation profiles in acute and chronic phases poststroke. Pro-inflammatory microglia exacerbate WMI via cytokine secretion and oligodendrocyte toxicity, while immune-regulatory microglia promote remyelination through trophic support and debris clearance. Key regulatory pathways include TREM2, CX3CR1, and purinergic signaling. Microglial phagocytosis, cytokine production, and interactions with astrocytes critically modulate remyelination. Therapeutic modulation of microglial phenotype (e.g., fingolimod, HDAC inhibitors) shows promise in enhancing white matter repair.
Conclusion:
Microglia exert time- and region-specific effects on WMI after ischemic stroke. A nuanced understanding of their dynamic phenotypes and interactions with other glial elements is essential for developing targeted therapies. Future research should integrate single-cell technologies, human validation, and sex-specific analyses to refine microglia-based interventions.
Insights
Microglia play a dual role in white matter injury following ischemic stroke, with distinct activation states influencing damage and repair. Understanding these dynamics is key to developing targeted therapies for neurological recovery.
Area of Science:
- Neuroscience
- Immunology
- Neuropathology
Background:
- Ischemic stroke often causes white matter injury (WMI), impairing neurological function.
- Microglia, the brain's immune cells, have a complex role in post-stroke WMI and recovery.
- Their activation states and glial interactions affect myelin damage and repair.
Purpose of the Study:
- To systematically review and synthesize evidence on microglia's temporal and functional roles in ischemic stroke-induced WMI.
- To focus on microglia's specific contributions to white matter damage and subsequent recovery.
Main Methods:
- Comprehensive literature search of PubMed, Web of Science, and Scopus databases (up to Dec 2024).
- Keywords: "ischemic stroke," "white matter injury," "microglia," "myelin," "oligodendrocytes."
- Prioritized studies on microglial polarization, myelin repair, and molecular pathways; included preclinical and clinical research.
Main Results:
- Microglia show distinct profiles in acute (pro-inflammatory, exacerbating WMI) and chronic (immune-regulatory, promoting remyelination) phases.
- Key pathways like TREM2, CX3CR1, and purinergic signaling regulate microglial function.
- Therapeutic strategies targeting microglial phenotypes show potential for enhancing white matter repair.
Conclusions:
- Microglia's effects on WMI post-stroke are time- and region-specific.
- Understanding dynamic microglial phenotypes and glial interactions is crucial for targeted therapies.
- Future research needs single-cell tech, human validation, and sex-specific analysis for refined interventions.
