Published online Aug 26, 2021. doi: 10.4252/wjsc.v13.i8.1030
Peer-review started: March 16, 2021
First decision: May 5, 2021
Revised: May 25, 2021
Accepted: August 6, 2021
Article in press: August 6, 2021
Published online: August 26, 2021
Processing time: 156 Days and 9 Hours
Inflammation plays an important role in the pathological process of ischemic stroke, and systemic inflammation affects patient prognosis. As resident immune cells in the brain, microglia are significantly involved in immune defense and tissue repair under various pathological conditions, including cerebral ischemia. Although the differentiation of M1 and M2 microglia is certainly oversimplified, changing the activation state of microglia appears to be an intriguing therapeutic strategy for cerebral ischemia. Recent evidence indicates that both mesenchymal stem cells (MSCs) and MSC-derived extracellular vesicles (EVs) regulate inflammation and modify tissue repair under preclinical stroke conditions. However, the precise mechanisms of these signaling pathways, especially in the context of the mutual interaction between MSCs or MSC-derived EVs and resident microglia, have not been sufficiently unveiled. Hence, this review summarizes the state-of-the-art knowledge on MSC- and MSC-EV-mediated regulation of microglial activity under ischemic stroke conditions with respect to various signaling pathways, including cytokines, neurotrophic factors, transcription factors, and microRNAs.
Core Tip: Upon stroke induction, M1 microglia participate in the proinflammatory tissue response, whereas M2 microglia promote brain repair by secreting anti-inflammatory cytokines and neurotrophic factors. This review summarizes the effects of mesenchymal stem cells (MSCs) and MSC-extracellular vesicles on regulating microglial activity under ischemic stroke conditions through various signaling pathways, such as cytokines, neurotrophic factors, transcription factors, and microRNAs.