Figure 1.

Cascades of the coagulation system. (a) Resting ECs provide natural anticoagulants (TM, AT and TFPI and ADPase) to inhibit coagulation and keep platelet activation and the coagulation cascade in check. (b) Coagulation is typically initiated by an injury to the vascular ECs, which results in the exposure of TF and collagen from the sub-endothelial tissue to the blood and the release of vWF. (c) Platelets are activated when they are exposed to TF, collagen and vWF. Activated platelets release a number of mediators, such as ADP and vWF stores within their granules, leading to further platelet recruitment, activation, aggregation and plug formation, which is a process termed primary hemostasis. (d) The interaction between TF and factor VII initiates the extrinsic pathway. (e) The exposure of collagen to blood starts the intrinsic pathway. (f) Both the extrinsic and intrinsic pathways result in the initiation of a common pathway, which contains the cascades involved in the production of activated Factor X and thrombin and the formation of fibrin strands. (g) Fibrin strands strengthen the platelet plug and lead to the formation of a stable platelet–fibrin clot. This process is termed secondary hemostasis. (h) Kallikrein, uPA or tPA activate plasminogen to plasmin, which then degrades and reabsorbs the polymerized fibrin strands. It is the eventual process of fibrinolysis that heals wounds. AT, antithrombin; ECs, endothelial cells; TF, tissue factor; TFPI, tissue factor pathway inhibitors; TM, thrombomodulin; tPA, tissue plasminogen activator; uPA, urokinase plasminogen activator; vWF, von Willebrand factor.