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Shear stress-induced platelet aggregation (SIPA) is a biological process in which platelets aggregate in response to high shear rates within the blood, particularly under pathological conditions such as vessel stenosis or turbulent flow. Unlike classical platelet aggregation, which is typically triggered by soluble agonists (e.g., ADP, thrombin), SIPA can occur without exogenous agonists and is primarily mediated by mechanical forces generated from blood flow. Key molecular players include von Willebrand Factor (vWF), Glycoprotein Ib (GPIb), and Glycoprotein IIb/IIIa. SIPA plays a crucial role in arterial thrombosis—especially at sites with disturbed or accelerated blood flow such as stenosed arteries—where it can lead directly to occlusive thrombus formation even without chemical agonists present. The process is highly relevant in cardiovascular diseases like myocardial infarction and stroke.
Inhibition of vWF multimerization or GPIb receptor cleavage
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