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Updated: Dec 23, 2025
Three-dimensional Confocal Analysis of Microglia/macrophage Markers of Polarization in Experimental Brain Injury
Published on: September 4, 2013
Modulators of microglia activation and polarization in ischemic stroke (Review)
Cheng-Ting Jiang1, Wan-Feng Wu1, Yi-Hui Deng1
1Hunan Province Key Laboratory of Cerebrovascular Disease Prevention and Treatment of Integrated Traditional Chinese and Western Medicine, College of Integrated Traditional Chinese and Western Medicine, Hunan University of Chinese Medicine, Changsha, Hunan 410208, P.R. China.
Abstract:
Ischemic stroke is one of the leading causes of mortality and disability worldwide. However, there is a current lack of effective therapies available. As the resident macrophages of the brain, microglia can monitor the microenvironment and initiate immune responses. In response to various brain injuries, such as ischemic stroke, microglia are activated and polarized into the proinflammatory M1 phenotype or the anti‑inflammatory M2 phenotype. The immunomodulatory molecules, such as cytokines and chemokines, generated by these microglia are closely associated with secondary brain damage or repair, respectively, following ischemic stroke. It has been shown that M1 microglia promote secondary brain damage, whilst M2 microglia facilitate recovery following stroke. In addition, autophagy is also reportedly involved in the pathology of ischemic stroke through regulating the activation and function of microglia. Therefore, this review aimed to provide a comprehensive overview of microglia activation, their functions and changes, and the modulators of these processes, including transcription factors, membrane receptors, ion channel proteins and genes, in ischemic stroke. The effects of autophagy on microglia polarization in ischemic stroke were also reviewed. Finally, future research areas of ischemic stroke and the implications of the current knowledge for the development of novel therapeutics for ischemic stroke were identified.
Insights
Microglia, the brain's immune cells, shift between M1 (harmful) and M2 (helpful) states after ischemic stroke. Understanding these microglia and autophagy is key to developing new stroke therapies.
Area of Science:
- Neuroscience
- Immunology
- Pathology
Background:
- Ischemic stroke is a major global cause of death and disability.
- Effective treatments for ischemic stroke remain limited.
- Microglia, brain-resident macrophages, play a critical role in the immune response to stroke.
Purpose of the Study:
- To provide a comprehensive overview of microglia activation, function, and modulation in ischemic stroke.
- To review the role of autophagy in microglia polarization and its impact on stroke outcomes.
- To identify future research directions and therapeutic implications for ischemic stroke.
Main Methods:
- Literature review focusing on microglia activation and polarization in ischemic stroke.
- Analysis of immunomodulatory molecules (cytokines, chemokines) produced by microglia.
- Examination of the influence of autophagy on microglia phenotype and function.
Main Results:
- Microglia polarization into M1 (pro-inflammatory) or M2 (anti-inflammatory) phenotypes significantly impacts stroke outcomes.
- M1 microglia exacerbate secondary brain damage, while M2 microglia promote recovery.
- Autophagy influences microglia activation and polarization, affecting the overall stroke pathology.
Conclusions:
- Modulating microglia polarization holds therapeutic potential for ischemic stroke.
- Targeting autophagy may offer a novel strategy to enhance beneficial M2 microglia responses.
- Further research into microglia-specific pathways is crucial for developing effective ischemic stroke treatments.
