Journal
SEMINARS IN THROMBOSIS AND HEMOSTASIS
Volume 37, Issue 3, Pages 305-314Publisher
THIEME MEDICAL PUBL INC
DOI: 10.1055/s-0031-1273094
Keywords
Deep vein thrombosis; factor XIII; factor XIII polymorphisms; pulmonary embolism; venous thromboembolism
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Funding
- Hungarian National Research Fund [OTKA-NKTH CNK80776]
- Hungarian Academy of Sciences [MTA 2006TKI227]
- Hungarian Ministry of Health [ETT2009, 460-06]
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Plasma factor XIII (FXIII) is a tetrameric zymogen consisting of two potentially active A subunits (FXIII-A) and two carrier/inhibitory B subunits (FXIII-B). In the final phase of the coagulation cascade, FXIII is converted into an active transglutaminase (FXIIIa) by thrombin and Ca2+. FXIIIa strengthens fibrin clot mechanically by cross-linking fibrin chains. In addition, FXIIIa is a key regulator of fibrinolysis, protecting newly formed fibrin from the fibrinolytic machinery by binding alpha(2)-plasmin inhibitor to the fibrin meshwork. FXIII is essential for maintaining hemostasis; its severe deficiency causes a life-threatening bleeding diathesis. The involvement of FXIII in thrombotic diseases and its association with the risk of these disorders is less clear. The role of FXIII in atherothrombotic diseases has been recently reviewed. This article offers a general overview of the relationship between FXIII and venous thromboembolism (VTE), to collect individual publications on this topic, present conclusions, and examine limitations of published studies. Special attention is given to the association of FXIII-A polymorphism with the risk of VTE, which has provoked considerable interest over the last decade.
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