General mechanisms of coagulation and targets of anticoagulants (Section I): Position Paper of the ESC Working Group on Thrombosis - Task Force on Anticoagulants in Heart Disease
2013 (English)In: Thrombosis and Haemostasis, ISSN 0340-6245, Vol. 109, no 4, 569-579 p.Article in journal (Refereed) Published
Contrary to previous models based on plasma, coagulation processes are currently believed to be mostly cell surface-based, including three overlapping phases: initiation, when tissue factor-expressing cells and microparticles are exposed to plasma; amplification, whereby small amounts of thrombin induce platelet activation and aggregation, and promote activation of factors (F)V, FVIII and FXI on platelet surfaces; and propagation, in which the Xase (tenase) and prothrombinase complexes are formed, producing a burst of thrombin and the cleavage of fibrinogen to fibrin. Thrombin exerts a number of additional biological actions, including platelet activation, amplification and self-inhibition of coagulation, clot stabilisation and anti-fibrinolysis, in processes occurring in the proximity of vessel injury, tightly regulated by a series of inhibitory mechanisms. "Classical" anticoagulants, including heparin and vitamin K antagonists, typically target multiple coagulation steps. A number of new anticoagulants, already developed or under development, target specific steps in the process, inhibiting a single coagulation factor or mimicking natural coagulation inhibitors.
Place, publisher, year, edition, pages
2013. Vol. 109, no 4, 569-579 p.
Medical and Health Sciences
IdentifiersURN: urn:nbn:se:uu:diva-197420DOI: 10.1160/TH12-10-0772ISI: 000317558100001PubMedID: 23447024OAI: oai:DiVA.org:uu-197420DiVA: diva2:612796