NETosis in ischemic stroke: Mechanisms, implications, and therapeutic prospects - PubMed
4 days ago
- #NETosis
- #Thromboinflammation
- #Ischemic stroke
- Ischemic stroke is a major global health issue with secondary injury mechanisms affecting long-term outcomes.
- NETosis, the formation of neutrophil extracellular traps, links immune activation with thrombotic and inflammatory damage in stroke.
- Neutrophils infiltrate ischemic tissue and undergo NETosis, releasing structures that interact with platelets, endothelial cells, and coagulation pathways.
- NET components promote thrombus formation, enhance stability, resist fibrinolysis, and worsen BBB breakdown and neuronal injury.
- NET-related markers like citrullinated histone H3 and MPO-DNA complexes correlate with stroke severity and poor recovery.
- Experimental NET-targeting strategies (DNase-I, PAD4 inhibition, MPO blockade) show neuroprotective effects in animal models.
- Translating NET-focused therapies to clinical practice is challenging due to patient diversity and comorbidities.
- NETosis contributes to stroke-related thrombosis, BBB disruption, and inflammation, highlighting potential for future therapies.