Figure - available from: Applied Rheology
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Schematic of the blood coagulation cascade. Activation of the coagulation cascade triggers the conversion of the inactive coagulation factors (represented by an F followed by a Roman number, e.g., FXII) to their active form (FXIIa) by a series of enzymatic reactions. The intrinsic pathway (purple) is also termed the “contact activation pathway,” which is activated by negatively charged surfaces, such as polyphosphates. The extrinsic pathway (orange) is initiated by TF that is released during vascular injury. The activation of platelets upon injury is not depicted here. The activation of coagulation factor ten (FX) marks the start of the common pathway (green) that leads to the formation of cross-linked fibrin clots.

Schematic of the blood coagulation cascade. Activation of the coagulation cascade triggers the conversion of the inactive coagulation factors (represented by an F followed by a Roman number, e.g., FXII) to their active form (FXIIa) by a series of enzymatic reactions. The intrinsic pathway (purple) is also termed the “contact activation pathway,” which is activated by negatively charged surfaces, such as polyphosphates. The extrinsic pathway (orange) is initiated by TF that is released during vascular injury. The activation of platelets upon injury is not depicted here. The activation of coagulation factor ten (FX) marks the start of the common pathway (green) that leads to the formation of cross-linked fibrin clots.

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The maintenance of hemostasis to ensure vascular integrity is dependent upon the rapid conversion of zymogen species of the coagulation cascade to their enzymatically active forms. This process culminates in the generation of the serine protease thrombin and polymerization of fibrin to prevent vascular leak at sites of endothelial cell injury or lo...