MicroRNAs as Potential Biomarkers and Therapeutic Targets in Ischemic Stroke from the Perspective of Inflammation.

Abstract

Ischemic stroke, triggered by the interruption of cerebral blood flow, initiates a complex inflammatory process involving both brain-resident and peripheral immune cells. Microglia, the primary brain-resident immune cells of high heterogeneity, regulate central nervous system inflammation upon activation. Activated microglia are commonly classified into two predominant phenotypes (pro-inflammatory M1 and anti-inflammatory M2), which exert dual effects through the secretion of distinct cytokine profiles. Peripheral immune cells, including monocytes, macrophages, and neutrophils, contribute to stroke pathogenesis and progression via diverse inflammatory mechanisms. Multiple microRNAs regulate the inflammatory dynamics of ischemic stroke across all phases by modulating both brain-resident and peripheral immune cells. MicroRNAs play a pivotal role in the activation and polarization of microglia, as well as cytokine release. Furthermore, microRNAs modulate the activation and extravasation processes of peripheral leukocytes by enhancing or attenuating signaling pathways. These mechanisms suggest that microRNA alterations could be biomarkers for predicting, diagnosing, and prognosticating ischemic stroke. Additionally, microRNA modulation offers potential as a therapeutic strategy for the treatment of ischemic stroke.