Platelet aggregation (for hemostasis)

Platelet aggregation for hemostasis is a physiological process in which activated platelets adhere to each other at sites of vascular injury, forming a platelet plug (hemostatic plug) to prevent blood loss. This process is vital for stopping bleeding, particularly in patients with thrombocytopenia or platelet dysfunction who receive platelet transfusions. Aggregation is mediated by several surface receptors—including ADP (P2Y12, P2Y1), thromboxane A2, and fibrinogen-binding glycoprotein IIb/IIIa—as well as extracellular ligands like collagen and thrombin. Numerous anti-platelet drugs target these pathways to modulate thrombosis risk in cardiovascular disease.

Other names

Platelet plug formationHemostatic plug formationPlatelet thrombus formation

Inhibition of cyclooxygenase-1 (aspirin): blocks thromboxane A2 synthesis Antagonism of P2Y12 ADP receptor (clopidogrel, ticagrelor, prasugrel): inhibits platelet activation and aggregation Inhibition of GP IIb/IIIa integrin (abciximab, eptifibatide, tirofiban): prevents fibrinogen-mediated platelet aggregation