New insights into factors affecting clot stability: A role for thrombin activatable fibrinolysis inhibitor (TAFI; plasma procarboxypeptidase B, plasma procarboxypeptidase U, procarboxypeptidase R).

The thrombin-catalyzed conversion of plasma fibrinogen into fibrin and the development of an insoluble fibrin clot are the final steps in the coagulation cascade during hemostasis. The delicate balance between clot formation and fibrinolysis, which determines clot stability, is controlled by a complex interplay between fibrin and other molecular and cellular components of the hemostatic system, including thrombin activatable fibrinolysis inhibitor (TAFI). TAFI is activated by thrombin and has an important role in the stability of the fibrin clot, which is reviewed here. In particular, the role of TAFI in fibrinolysis and those characteristics of the protein that affect clot stability are described. In addition, the importance of TAFI in the coagulation process and how changes in its availability may contribute to bleeding or thrombotic disorders are discussed.