Prothrombotic Platelets: Unlocking a New Mechanism in Antiphospholipid Syndrome
A new study in *Arthritis & Rheumatology* reveals a key molecular driver of thrombosis in antiphospholipid syndrome (APS). 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 via calcium-dependent signaling in a self-reinforcing loop. The prothrombotic effect was directly linked to antiphospholipid antibodies, as control platelets exposed to APS IgG showed enhanced PANX1 phosphorylation and ATP release. Crucially, the PANX1 inhibitor carbenoxolone normalized ATP release and reduced platelet activation markers like P-selectin expression and aggregation, suggesting PANX1 channels as a novel therapeutic target to restore platelet homeostasis without impairing hemostasis.
Why it might matter to you:
This research provides a clear cellular and molecular pathology for a major thrombotic disorder, directly linking a diagnostic antibody to a specific dysregulated channel and signaling pathway. For pathologists and clinical laboratories, it identifies PANX1 activity and ATP release as potential functional biomarkers for assessing thrombotic risk in APS patients. The findings could guide the development of more targeted diagnostic panels and inform the evaluation of new antiplatelet therapies that aim to modulate this specific pathway, moving beyond broad anticoagulation.
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