Microglial Polarization: Novel Therapeutic Strategy against Ischemic Stroke

Abstract

Ischemic stroke, which is the second highest cause of death and the leading cause of disability, represents ~71% of all strokes globally. Some studies have found that the key elements of the pathobiology of stroke is immunity and inflammation. Microglia are the first line of defense in the nervous system. After stroke, the activated microglia become a double-edged sword, with distinct phenotypic changes to the deleterious M1 types and neuroprotective M2 types. Therefore, ways to promote microglial polarization toward M2 phenotype after stroke have become the focus of attention in recent years. In this review, we discuss the process of microglial polarization, summarize the alternation of signaling pathways and epigenetic regulation that control microglial polarization in ischemic stroke, aiming to find the potential mechanisms by which microglia can be transformed into the M2 polarized phenotype.

Keywords: cell polarization; ischemic stroke; mechanism; microglia; treatment.

Figure 1.

Microglia polarization after ischemic stroke. M1 microglia produce pro-inflammatory cytokines to exacerbate neural death, astrocyte apoptosis, and blood brain barrier (BBB) disruption. Conversely, M2 microglia produce anti-inflammatory cytokines to maintain BBB integrity, promote the proliferation and differentiation of neural cells and tissue repair.