A Thrombotic Switch: How Platelet Channels Fuel Clots in Antiphospholipid Syndrome
A new study in *Arthritis & Rheumatology* reveals a key mechanism driving thrombosis in antiphospholipid syndrome (APS), an autoimmune condition notorious for causing blood clots. Researchers found that platelets from APS patients exhibit abnormally high basal release of ATP, a pro-thrombotic signaling molecule. This release occurs through specialized channels called pannexin-1 (PANX1). Crucially, antibodies from APS patients were shown to activate these PANX1 channels, leading to a cascade of platelet activation, aggregation, and P-selectin expression—all critical steps in clot formation. The process is dependent on calcium signaling and activation of P2X1 receptors by the released ATP. Importantly, inhibiting the PANX1 channel with the drug carbenoxolone significantly reduced this pathological platelet hyperactivity.
Why it might matter to you: For cardiologists managing cardiovascular risk in complex autoimmune patients, this research identifies PANX1 as a novel and targetable pathway for thrombosis. Current antiplatelet therapies carry bleeding risks, but a channel blocker like carbenoxolone could potentially disrupt clot formation in APS without broadly impairing hemostasis. This points toward future, more precise therapeutic strategies for preventing myocardial infarction, stroke, and other thrombotic events in this high-risk population, moving beyond traditional anticoagulation.
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