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.

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.