Ischemic stroke is one of the leading causes of death and disability globally, but its treatment options are limited due to therapeutic window and reperfusion injury constraints. Microglia, astrocytes, and oligodendrocytes are the major components of the neurovascular unit, and there is substantial evidence suggesting their contributions to maintaining homeostasis in the central nervous system. Neuroglial cells participate in neuronal physiological functions and the repair of damaged neurons through various communication methods, including gap junctions, chemical signaling, and extracellular vesicles, in conjunction with other components of the neurovascular unit. Ischemia-induced microglia and astrocytes polarize into "M1/M2" and "A1/A2" phenotypes and exert neurotoxic or neuroprotective effects by releasing soluble factors, secreting extracellular vesicles, and forming syncytia networks in the acute (<72 h), subacute (>72 h), and chronic phases (>6 weeks). Apoptosis of oligodendrocytes due to ischemic hypoxia leads to white matter injury, causing long-term cognitive dysfunction, and promoting oligodendrogenesis is a crucial direction for achieving functional recovery in ischemic stroke. In this article, we summarize the cellular interactions following cerebral ischemia, analyze the roles of neuroglial cells through gap junctions, chemical signaling, and extracellular vesicles in different stages of ischemic stroke, and further explore strategies for intervening in ischemic stroke.
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| http://dx.doi.org/10.1016/j.brainresbull.2024.110910 | DOI Listing |
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