Abstract
Ischemic brain injuries are common diseases with high morbidity, disability, and mortality rates, which have significant impacts on human health and life. Microglia are resident cells of the central nervous system (CNS). The inflammatory responses mediated by microglia play an important role in the occurrence and development of ischemic brain injuries. This article summarizes the activation, polarization, depletion, and repopulation of microglia after ischemic brain injuries, proposing new treatment strategies for such injuries through the modulation of microglial function.
Highlights
Ischemic brain injuries mainly contain ischemic stroke, cerebral white-matter ischemia, and neonatal hypoxia-ischemic brain damage, which are the third-leading cause of human disability, and the second-leading cause of death in the world (Desmond et al, 2002; Candelario-Jalil, 2009; Mozaffarian et al, 2016)
There is a close relationship between microglial function and the pathogenesis of ischemic brain injuries
M2 microglia can promote the expression of anti-inflammatory cytokines and neurotrophic factors, thereby alleviating ischemic brain injuries
Summary
Ischemic brain injuries mainly contain ischemic stroke, cerebral white-matter ischemia, and neonatal hypoxia-ischemic brain damage, which are the third-leading cause of human disability, and the second-leading cause of death in the world (Desmond et al, 2002; Candelario-Jalil, 2009; Mozaffarian et al, 2016). This article summarizes the roles of microglia in the pathogenesis of ischemic brain injuries and proposes new treatment strategies through the modulation of microglial function. ACTIVATION, PROLIFERATION, AND MIGRATION OF MICROGLIA AFTER ISCHEMIC BRAIN INJURIES
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