The hemostatic process. Upon vessel injury, platelets roll and become tethered to the vessel wall by interactions with vWF and collagen (noted as black strands). These interactions cause platelet shape change, and release of ADP from dense granules. The activated platelet also generates thromboxane A₂ (TxA₂). Both ADP and TxA₂ are agonists that cause further platelet activation and accumulation of platelets at the site of injury. Vessel injury also causes exposure of tissue factor, which catalyzes the coagulation response. This response results in the formation of thrombin, which further activates platelets and cleaves fibrinogen to form fibrin. The combination of activated platelets and fibrin at the site of injury forms a stable hemostatic plug that arrests bleeding.