Cerebral ischemic stroke is a disease that belongs to the group of acute vascular disorders of the cerebral circulation. It is considered a major cause of disability and mortality worldwide. It has been shown that the integrity of the blood-brain barrier is impaired after an ischemic stroke, and this is the key factor in brain damage. An inflammatory reaction occurs, which is provoked and maintained by bioactive substances released by endothelial cells, brain glial cells, and blood immune cells. Microglial cells are the first to respond to an injury; they get activated through a series of molecular mechanisms and transformed into diverse functional subtypes. Activated microglia can have both aggravating and beneficial effects regarding tissue remodeling and recovery after ischemia. In addition to their functions, activated microglial cells also differ in their morphology, gene expression, and protein profile. Their type can also vary depending on the distance from the ischemic lesion. Microglial plasticity, as well as the complex relationships of microglia with other cells in the central nervous system under physiological conditions and after ischemic stroke, have been studied mainly in experimental animals: rodents and primates. However, more information has been generated by in vivo studies of post-stroke patients, applying highly specialized imaging methods. Nevertheless, the obtained results are insufficient and ambiguous, but they are a good basis for developing strategies to influence the recovery process after ischemic brain injury.
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