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Semin Thromb Hemost 1999; 25(4): 419-428
DOI: 10.1055/s-2007-994944
Copyright © 1999 by Thieme Medical Publishers, Inc.

The Role of Factor XI in Coagulation: A Matter of Revision

Monique C. Minnema† , Hugo ten Cate† ‡ , C. Erik Hack
  • Laboratory for Clinical and Experimental Immunology, Central Laboratory of the Netherlands Red Cross Blood Transfusion Service;
  • †Center for Hemostasis, Thrombosis, Atherosclerosis and Inflammation Research, Academic Medical Center;
  • ‡Department of Internal Medicine, Slotervaart Hospital, Amsterdam, The Netherlands
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Publikationsdatum:
06. Februar 2008 (online)

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Abstract

In 1991 it was demonstrated that, besides factor XII, thrombin is capable of activating factor XI in vitro. Thrombin-dependent activation of factor XI is an integral part of the revised theoretical model of coagulation in which coagulation is initiated by the extrinsic pathway and maintained by thrombin-induced activation of clotting factors V, VIII, and XI. In this review, special interest is given to the new role of factor XI in coagulation, with emphasise on data supporting the concept of thrombin-mediated factor XI activation in vivo. Furthermore, activation of factor XI in human disease, especially atherosclerotic disease, measured by newly developed immunologic assays, is discussed. The relation of factor XI to fibrinolysis through activation of the carboxypeptidase, thrombin-activatable fibrinolysis inhibitor (TAFI) by thrombin provides an explanation for the bleeding tendency observed in factor Xl-deficient patients. The probable link with factor XI-mediated TAFI activation may have clinical and therapeutic consequences and deserves further study.

Keywords:

Factor XI - contact activation - coagulation - TAFI - factor XI deficiency

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