| Literature DB >> 33815877 |
Yimeng Xue1,2, Ding Nie1, Lin-Jian Wang1,2, Han-Cheng Qiu1, Long Ma1, Ming-Xin Dong3, Wen-Jun Tu1,3, Jizong Zhao1,2,4,5,6.
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. copyright:Entities:
Keywords: cell polarization; ischemic stroke; mechanism; microglia; treatment
Year: 2021 PMID: 33815877 PMCID: PMC7990355 DOI: 10.14336/AD.2020.0701
Source DB: PubMed Journal: Aging Dis ISSN: 2152-5250 Impact factor: 6.745