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TREM2-mediated regulation of microglial activity: a promising target for the treatment of ischemic stroke
Haihan Yu1, Li Zhang2, Bo Song1
1Department of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, P. R. China.
Abstract:
Ischemic stroke, the most prevalent type of stroke globally, poses significant challenges due to its high incidence, morbidity, and long-term disability. Microglia, the resident immune cells of the central nervous system (CNS), play a dual role in the context of ischemic stroke. While they contribute to neuroinflammation by releasing pro-inflammatory cytokines and exacerbating neuronal injury, they also facilitate tissue repair, angiogenesis, and restoration of the blood-brain barrier (BBB) integrity through the secretion of anti-inflammatory and neurotrophic factors. Triggering receptor expressed on myeloid cells 2 (TREM2), predominantly expressed on microglia, is a critical regulator of microglial proliferation, survival, phagocytosis, polarization, inflammation, and metabolism. TREM2 has emerged as a key modulator of immune responses in ischemic stroke. This review provides a comprehensive examination of the multifaceted roles of TREM2 in microglial biology during ischemic stroke, integrating current insights into its molecular mechanisms. Furthermore, it highlights TREM2's potential as a transformative therapeutic target, advancing our understanding of neuroimmune regulation and promoting recovery after stroke.
Insights
Triggering receptor expressed on myeloid cells 2 (TREM2) influences microglial function in ischemic stroke. Understanding TREM2
Area of Science:
- Neuroscience
- Immunology
- Stroke Research
Background:
- Ischemic stroke is a leading cause of disability worldwide.
- Microglia, the CNS immune cells, have dual roles in stroke pathology.
- Triggering receptor expressed on myeloid cells 2 (TREM2) is crucial for microglial function.
Purpose of the Study:
- To review the multifaceted roles of TREM2 in microglial biology during ischemic stroke.
- To explore the molecular mechanisms of TREM2 in neuroinflammation and repair.
- To highlight TREM2 as a potential therapeutic target for stroke recovery.
Main Methods:
- Comprehensive literature review of TREM2 in ischemic stroke.
- Analysis of TREM2's regulation of microglial proliferation, survival, and polarization.
- Integration of current insights into TREM2's molecular mechanisms.
Main Results:
- TREM2 critically regulates microglial responses, including inflammation and phagocytosis.
- TREM2 influences neuroinflammation, tissue repair, and blood-brain barrier integrity.
- TREM2 acts as a key modulator of immune responses in the context of ischemic stroke.
Conclusions:
- TREM2 plays a complex, dual role in ischemic stroke, impacting both injury and repair.
- Targeting TREM2 offers a promising therapeutic strategy for stroke treatment.
- Further research into TREM2's mechanisms can advance neuroimmune regulation and stroke recovery.
Related Concept Videos
Ischemic Stroke l: Introduction
Ischemic Stroke ll: Pathophysiology

