In brief, our latest findings indicate that P2X1 receptors contribute to ATP-dependent thrombosis in mouse microcirculation by promoting early neutrophil and platelet recruitment and subsequent fibrin generation, locally, at the sites of endothelial injury.
Upon systemic inflammatory challenge, P2X1 receptors would act to dampen the activation of circulating neutrophils, thereby limiting oxidative tissue damage and disseminated intravascular coagulation.
Targeting P2X1 receptors will not only inhibit platelets but also alter neutrophil function, and may therefore represent an innovative therapeutic strategy to prevent local thrombo-inflammation, only if neutrophil regulatory homeostasis is preserved.
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