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Published on: June 20, 2025
Complex Roles of Microglial Cells in Ischemic Stroke Pathobiology: New Insights and Future Directions
Revathy Guruswamy1,2, Ayman ElAli3,4
1Neuroscience Axis, CHU de Québec Research Center (CHUL), Québec City, QC G1V 4G2, Canada. revathy.guruswamy.1@ulaval.ca.
Abstract:
Ischemic stroke constitutes the major cause of death and disability in the industrialized world. The interest in microglia arose from the evidence outlining the role of neuroinflammation in ischemic stroke pathobiology. Microglia constitute the powerhouse of innate immunity in the brain. Microglial cells are highly ramified, and use these ramifications as sentinels to detect changes in brain homeostasis. Once a danger signal is recognized, cells become activated and mount specialized responses that range from eliminating cell debris to secreting inflammatory signals and trophic factors. Originally, it was suggested that microglia play essentially a detrimental role in ischemic stroke. However, recent reports are providing evidence that the role of these cells is more complex than what was originally thought. Although these cells play detrimental role in the acute phase, they are required for tissue regeneration in the post-acute phases. This complex role of microglia in ischemic stroke pathobiology constitutes a major challenge for the development of efficient immunomodulatory therapies. This review aims at providing an overview regarding the role of resident microglia and peripherally recruited macrophages in ischemic pathobiology. Furthermore, the review will highlight future directions towards the development of novel fine-tuning immunomodulatory therapeutic interventions.
Insights
Microglia, the brain's immune cells, have a dual role in ischemic stroke. They are detrimental in the acute phase but essential for tissue repair later, complicating immunomodulatory therapies.
Area of Science:
- Neuroscience
- Immunology
- Pathobiology
Background:
- Ischemic stroke is a leading cause of death and disability.
- Neuroinflammation, driven by microglia, plays a critical role in stroke pathology.
- Microglia, the brain's innate immune cells, act as sentinels for homeostasis.
- Their activation leads to responses including debris clearance and inflammatory signaling.
Purpose of the Study:
- To review the complex role of microglia and macrophages in ischemic stroke.
- To explore the dual function of microglia in acute and post-acute stroke phases.
- To highlight future directions for immunomodulatory therapeutic interventions.
Main Methods:
- Literature review of scientific reports on microglia and ischemic stroke.
- Analysis of the evolving understanding of microglial roles.
- Identification of challenges and opportunities in immunomodulatory therapy development.
Main Results:
- Microglia exhibit a complex, dual role in ischemic stroke.
- Initially considered detrimental, microglia are now recognized as crucial for tissue regeneration post-stroke.
- This complexity presents a challenge for developing effective immunomodulatory treatments.
Conclusions:
- The multifaceted role of microglia in ischemic stroke necessitates nuanced therapeutic strategies.
- Understanding the temporal dynamics of microglial activation is key for future interventions.
- Targeting microglia and macrophages offers potential for novel stroke therapies.
