ArticleJournal of neuroinflammation2025
Targeting hypercoagulability in ischemic stroke modulates fibrin-driven microglial polarization via JAK-STAT pathway.
Article in Journal of neuroinflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- Astrocyte-Microglia Crosstalk in Post-Hemorrhagic Neurovascular Microenvironment: Mechanistic Nodes, Cross-Stroke Comparisons, and Therapeutic Reprogramming.Translational stroke research · 2026Review
- Fibrinogen in extracellular matrix remodeling: functional switching, source heterogeneity, and biomaterial translation.Frontiers in cell and developmental biology · 2026Review
- β-Caryophyllene protects against ischemic stroke by inhibiting H3K9 and H3K18 lactylation-mediated cellular pyroptosis.Frontiers in pharmacology · 2026Article
- Inflammation-centered neurovascular-immune-metabolic remodeling in ischemic stroke: stage-dependent mechanisms, regulated cell death, and therapeutic translation.Frontiers in immunology · 2026Review
- Salvianolic acid B alleviates depression-like behaviors by reducing neuronal injury and promoting neurogenesis in a manner associated with JAK-STAT signaling pathway inhibition.Frontiers in neurologyArticle
Corrections and comments
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Authors and funding
9 authors.
Funding
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 ITGB2 on primary microglia and activates the JAK-STAT signaling pathway, influencing microglial polarization. These results establish a novel link between the hypercoagulable state and microglial function, offering a promising therapeutic approach to reduce neuroinflammation, improve neurological function and enhance outcomes in ischemic stroke by targeting coagulation pathways.
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Registered trials
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