Astrogliosis and glial scar in ischemic stroke - focused on mechanism and treatment

Abstract

Ischemic stroke is a kind of neurological dysfunction caused by cerebral ischemia. Astrocytes, as the most abundant type of glial cells in the central nervous system, are activated into reactive astrocytes after cerebral ischemia, and this process involves the activation or change of a series of cell surface receptors, ion channels and ion transporters, GTPases, signaling pathways, and so on. The role of reactive astrocytes in the development of ischemic stroke is time-dependent. In the early stage of ischemia, reactive astrocytes proliferate moderately and surround the ischemic tissue to prevent the spread of the lesion. At the same time, reactive astrocytes release neuroprotective factors, ultimately relieving brain injury. In the late stage of ischemia, reactive astrocytes excessively proliferate and migrate to form dense glial scar tissue, which hinders the repair of damaged tissue. At the same time, reactive astrocytes in the glial scar release a large number of neurotoxic factors, ultimately aggravating ischemic stroke. In this paper, we focus on the molecular mechanism of astrogliosis and glial scar formation after cerebral ischemia, and explore the relevant studies using glial scar as a therapeutic target, providing a reference for the selection of therapeutic strategies for ischemic stroke and further research directions.