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Platelet adhesion and aggregation are the sequential processes by which platelets respond to vascular injury to form a physical plug. Adhesion is the initial tethering of platelets to the exposed subendothelial matrix, mediated by interactions between platelet receptors (like GP Ib-IX-V and GP VI) and ligands such as von Willebrand factor and collagen (StatPearls, 2023). This is followed by activation and aggregation, where platelets change shape and release agonists (ADP, Thromboxane A2) that recruit more platelets, eventually cross-linking via the Glycoprotein IIb/IIIa receptor and fibrinogen (NIH, 2005). While vital for preventing blood loss, these processes are central to the pathogenesis of arterial thrombosis, leading to conditions like myocardial infarction and stroke (Nature Reviews Cardiology, 2013). Consequently, various components of these pathways are major therapeutic targets for antiplatelet drugs, which aim to reduce thrombotic risk while balancing the inherent risk of bleeding (Mayo Clinic, 2023).
Inhibition of platelet activation and recruitment through various pathways, including COX-1 inhibition, P2Y12 receptor antagonism, Glycoprotein IIb/IIIa receptor blockade, and PAR-1 antagonism.
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