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How it all starts: Initiation of the clotting cascade.

Authors: Smith, SA  Travers, RJ  Morrissey, JH 
Citation: Smith SA, etal., Crit Rev Biochem Mol Biol. 2015;50(4):326-36. doi: 10.3109/10409238.2015.1050550. Epub 2015 May 28.
Pubmed: (View Article at PubMed) PMID:26018600
DOI: Full-text: DOI:10.3109/10409238.2015.1050550

The plasma coagulation system in mammalian blood consists of a cascade of enzyme activation events in which serine proteases activate the proteins (proenzymes and procofactors) in the next step of the cascade via limited proteolysis. The ultimate outcome is the polymerization of fibrin and the activation of platelets, leading to a blood clot. This process is protective, as it prevents excessive blood loss following injury (normal hemostasis). Unfortunately, the blood clotting system can also lead to unwanted blood clots inside blood vessels (pathologic thrombosis), which is a leading cause of disability and death in the developed world. There are two main mechanisms for triggering the blood clotting, termed the tissue factor pathway and the contact pathway. Only one of these pathways (the tissue factor pathway) functions in normal hemostasis. Both pathways, however, are thought to contribute to thrombosis. An emerging concept is that the contact pathway functions in host pathogen defenses. This review focuses on how the initiation phase of the blood clotting cascade is regulated in both pathways, with a discussion of the contributions of these pathways to hemostasis versus thrombosis.


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CRRD Object Information
CRRD ID: 11342779
Created: 2016-07-06
Species: All species
Last Modified: 2016-07-06
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.