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Updated: Oct 8, 2025

Isolation and Flow Cytometric Assessment of Neuroimmune Interactions in a Mini-Stroke Murine Model
Published on: June 20, 2025
[Dual roles and mechanism of microglia in ischemic stroke]
Ming-Xing Cheng1, Chen-Hui Li1, Wei Meng2
1State Key Laboratory of Natural Medicines, School of Life Science and Technology, China Pharmaceutical University, Nanjing 211198, China.
Abstract:
Stroke is the second most common cause of death after cancer worldwide and a major cause of acquired disability in adults. Overwhelming majority of strokes are caused by cerebral ischemia and are classified as ischemic stroke. Microglia are the resident immune cells and play dual roles in response to ischemia injury in the central nervous system (CNS). On the one hand, microglia may contribute to tissue function recovery process by promoting inflammation resolution, cellular debris clearance, nerve regeneration and synapse remodeling. On the other hand, excessive activation of microglia aggravates nerve damage after ischemic injury. Here, we briefly describe the mechanism of microglia activation after stroke, and comprehensively review the dual role of microglia in neurodegeneration and regeneration after stroke. In-depth exploration of the cytotoxic and protective mechanisms of microglia will provide new targets and new strategies for stroke treatment.
Insights
Microglia, the brain's immune cells, have a dual role in stroke recovery. Understanding their protective and damaging mechanisms offers new therapeutic targets for ischemic stroke treatment.
Area of Science:
- Neuroscience
- Immunology
- Pathology
Background:
- Stroke is a leading global cause of death and disability.
- Ischemic stroke, caused by cerebral ischemia, accounts for the vast majority of strokes.
- Microglia, the central nervous system's resident immune cells, exhibit complex responses to ischemic injury.
Purpose of the Study:
- To review the dual role of microglia in neurodegeneration and regeneration following stroke.
- To elucidate the mechanisms underlying microglia activation after ischemic stroke.
- To identify potential therapeutic targets based on microglia's cytotoxic and protective functions.
Main Methods:
- Literature review of studies on microglia activation and function post-stroke.
- Analysis of mechanisms involved in microglia-mediated neuroinflammation and neuroprotection.
- Synthesis of current understanding of microglia's impact on stroke outcomes.
Main Results:
- Microglia activation following stroke can be both detrimental, exacerbating nerve damage, and beneficial, promoting tissue repair.
- Key mechanisms include inflammation resolution, debris clearance, nerve regeneration, and synapse remodeling.
- Excessive or dysregulated microglial activation contributes to secondary injury.
Conclusions:
- Microglia present a "double-edged sword" in the context of ischemic stroke.
- Targeting specific microglial pathways could mitigate neurodegeneration and enhance functional recovery.
- Further research into microglia's multifaceted roles is crucial for developing novel stroke therapies.

