Abstract

A delicate balance between coagulation and fibrinolysis determines the stability of the fibrin clot. A Thrombin Activatable Fibrinolysis Inhibitor (TAFI) plays important role in this process. Activated by thrombin TAFI (TAFIa) also described as plasma carboxypeptidase B, carboxipeptidase U and carboxipeptidase R, inhibits fibrinolysis by removing carboxy-terminal lysine residues from fibrin.

Elimination of these lysines abrogates the fibrin cofactor function of t-PA-mediated plasminogen activation resulting in a decreased rate of plasmin generation and thus down regulation of fibrinolysis. The role of TAFI in bleeding and thrombotic disorders is discussed as well as its novel emerging role in inflammation.

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