Schematic overview of LRRC8 activation and ATP-release with subsequent platelet activation, thrombo-occlusion, and clinical manifestation upon mechanical shear stress. Although in resting platelets the LRRC8 complex (VRAC) is inactive, mechanical shear stress at the sites of atherosclerotic stenosis or plaque rupture mediates LRRC8-dependent release of ATP with subsequent autocrine and paracrine platelet activation via purinergic (P2X1, P2Y12) signaling. Shear-induced platelet activation leads to clot formation and cardiovascular disorders, such as thrombosis, ischemic stroke, and myocardial thromboinflammation, which is potentially averted by pharmacologic LRRC8 inhibition. The figure was created with BioRender.com. Münzer P. (2025) https://biorender.com/72ra0hf.

Schematic overview of LRRC8 activation and ATP-release with subsequent platelet activation, thrombo-occlusion, and clinical manifestation upon mechanical shear stress. Although in resting platelets the LRRC8 complex (VRAC) is inactive, mechanical shear stress at the sites of atherosclerotic stenosis or plaque rupture mediates LRRC8-dependent release of ATP with subsequent autocrine and paracrine platelet activation via purinergic (P2X1, P2Y12) signaling. Shear-induced platelet activation leads to clot formation and cardiovascular disorders, such as thrombosis, ischemic stroke, and myocardial thromboinflammation, which is potentially averted by pharmacologic LRRC8 inhibition. The figure was created with BioRender.com. Münzer P. (2025) https://biorender.com/72ra0hf.

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