Targeting hypercoagulability in ischemic stroke modulates fibrin-driven microglial polarization via JAK-STAT pathway.

ABSTRACT: Ischemic stroke is a leading cause of mortality and disability worldwide, yet its pathophysiological mechanisms remain poorly understood. In this study, we analyzed the coagulation function in 60 patients with acute ischemic stroke and found that their blood was in a hypercoagulable state. We confirmed this hematological change using a middle cerebral artery occlusion/reperfusion (MCAO/r) mouse model and improved the hypercoagulable state with the synthetic peptide Arg-Gly-Asp-Cys (RGDC), which inhibits platelet aggregation and fibrinogen binding. Interestingly, in MCAO/r mice, RGDC treatment led to enhanced neurological function, reduced blood-brain barrier (BBB) disruption, and alleviated neuroinflammation. Further analysis revealed that fibrin, the end product of coagulation, binds to I

SUBMITTER: Guan S 

PROVIDER: S-EPMC12584507 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature