Figure 1.

Overview of mechanisms of hemostasis. The coagulation cascade during hemostasis is initiated with the release of tissue factor (TF). (1) At the site of endothelial injury, TF that is stored in the adventitial and medial layers of the vessel wall is released. Platelet activation and adhesion occurs at the site of injury. (1) Encrypted TF is also released from monocyte-derived microparticles. Encrypted TF is activated through the secretion of protein disulfide isomerase (PDI), which occurs because of endothelial injury and platelet activation. (2) Activated TF will form a complex with circulating factor VIIa (FVIIa), leading to activation of FX to FXa. A small amount of thrombin generated creates an amplification loop by activating FVIII, FXI, and FV. (3) During the propagation phase, FIXa, which is generated by TF–VIIa complex or FXIa, binds to its cofactor FVIIIa to form the intrinsic tenase complex. FXa is then formed by TF–FVIIa complex or FIXa–FVIIa complex. (4) FXa binds to FVa, forming the prothrombinase complex. (5) FXa–FVa complex converts prothrombin to thrombin. (6) Thrombin further activates fibrinogen to fibrin, which is cross-linked by FXIIIa to form a stable clot.