A New Prothrombotic Pathway Emerges in Antiphospholipid Syndrome
A study in *Arthritis & Rheumatology* reveals a novel mechanism driving thrombosis in antiphospholipid syndrome (APS), an acquired autoimmune disorder characterized by clotting and pregnancy complications. Researchers found that platelets from APS patients exhibit significantly higher basal release of ATP through pannexin-1 (PANX1) channels. This ATP then activates P2X receptors, amplifying platelet activation through calcium-dependent signaling in a self-reinforcing loop. The prothrombotic effect was directly linked to patient-derived antiphospholipid antibodies, which enhanced PANX1 phosphorylation, ATP release, and platelet aggregation—effects that were blocked by the PANX1 inhibitor carbenoxolone and calcium chelation.
Why it might matter to you:
This research identifies PANX1 channels as a specific, druggable target within the coagulation cascade for a high-thrombosis-risk population. For hematologists focused on bleeding and clotting disorders, it suggests a potential new therapeutic strategy that could inhibit pathological thrombosis in APS without broadly impairing hemostasis. The findings underscore the importance of platelet signaling pathways beyond traditional anticoagulation, pointing toward future precision therapies for autoimmune-related thrombosis.
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