Semin Thromb Hemost 2011; 37(3): 305-314
DOI: 10.1055/s-0031-1273094
© Thieme Medical Publishers

Factor XIII and Venous Thromboembolism

Zsuzsanna Bereczky1 , László Muszbek1
  • 1Clinical Research Center and Thrombosis, Haemostasis and Vascular Biology Research Group of the Hungarian Academy of Sciences, University of Debrecen, Medical and Health Science Center, Debrecen, Hungary
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Publikationsverlauf

Publikationsdatum:
31. März 2011 (online)

ABSTRACT

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 α2-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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László MuszbekM.D. Ph.D. 

Clinical Research Center, University of Debrecen, Medical and Health Science Center

P.O. Box 40, H-4012 Debrecen, Hungary

eMail: muszbek@med.unideb.hu