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. 2017 Apr 12;18(4):809. doi: 10.3390/ijms18040809

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© 2017 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Extrinsic coagulation cascade initiated by tissue factor (TF)-activated coagulation factor VII (fVIIa) dimer formation on the surface of extravascular cells. The TF-fVIIa complex triggers calcium ion-dependent sequential enzymatic reactions in response to injury of blood vessels composed of endothelial cells and the vessel wall. Formation of fibrin polymers together with platelets and red blood cells leads to clot formation to halt bleeding. This fibrin deposition process is supported by von Willebrand factors (vWFs). Blood coagulation completes by clot formation with other factors, such as platelets and red blood cells. Schematics of fibrin(ogen) with characteristic domains D and E are also shown. fXa: activated factor X; flXa: activated fIX; : cleavage; : conversion.

Inline graphic — Extrinsic coagulation cascade initiated by tissue factor (TF)-activated coagulation factor VII (fVIIa) dimer formation on the surface of extravascular cells. The TF-fVIIa complex triggers calcium ion-dependent sequential enzymatic reactions in response to injury of blood vessels composed of endothelial cells and the vessel wall. Formation of fibrin polymers together with platelets and red blood cells leads to clot formation to halt bleeding. This fibrin deposition process is supported by von Willebrand factors (vWFs). Blood coagulation completes by clot formation with other factors, such as platelets and red blood cells. Schematics of fibrin(ogen) with characteristic domains D and E are also shown. fXa: activated factor X; flXa: activated fIX; : cleavage; : conversion.