Dual Regulatory Role of Microglia in Myelin Repair After Stroke

doi:10.3969/j.issn.1009-0126.2025.04.032

Abstract：Stroke is one of the leading causes of global death and disability, and the second leading cause of death worldwide. In China, ischemic stroke (IS) accounts for more than 80% of stroke cases [1-2]. After IS, white matter is damaged, leading to demyelination and affecting neural function. Oligodendrocytes are components of myelin, and they are prone to degeneration after IS due to hypoxia and nutrient deficiency. Recent studies have shown that regulating myelin regeneration is an important approach for neuroprotection, promoting brain functional recovery, and white matter repair in IS. Microglia are resident immune cells in the central nervous system. When IS occurs, damage-associated molecular patterns are released in the area of cerebral infarction, and microglia in a steady state are activated within minutes, showing high heterogeneity, and play a dual regulatory role in myelin regeneration [4]. Evidence has shown that microglia regulate the migration, differentiation, and maturation of oligodendrocyte precursor cells (OPCs) through multiple pathways, participating in myelin regeneration. However, high inflammatory states, inflammatory aging, and aged microglia, due to impaired function, affect OPC function and hinder myelin regeneration. This review systematically analyzes the regulatory role of microglia in myelin repair after IS and summarizes measures to promote myelin regeneration by targeting microglia, providing new insights for clinical translation.