Thrombin Activatable Fibrinolysis Inhibitor (TAFI) is a protein involved in the control and regulation of blood clotting and fibrinolysis processes. It is synthesized and released by platelets, liver cells, and endothelial cells lining blood vessels.
TAFI plays a crucial role in maintaining the balance between blood clot formation and dissolution. When blood vessel injury occurs and bleeding starts, thrombin is activated. Thrombin mediates the conversion of fibrinogen into fibrin, forming a stable blood clot. Simultaneously, thrombin activates TAFI, transforming it into its active form called activated TAFI (TAFIa).
The main function of TAFIa is to inhibit fibrinolysis, which is the process of breaking down and dissolving blood clots. TAFIa acts by binding to and inhibiting different components of the fibrinolytic system, such as plasminogen and tissue plasminogen activator (tPA). By doing so, TAFIa reduces the generation of plasmin, which is responsible for clot dissolution.
This inhibition of fibrinolysis by TAFIa helps maintain the stability and integrity of blood clots, preventing excessive bleeding. However, an overactive TAFI system can lead to increased clot formation and a higher risk of thrombotic events, such as deep vein thrombosis or stroke.
Understanding the role of TAFI and its interactions with other components of the coagulation and fibrinolysis systems is crucial for developing strategies to regulate blood clot formation and dissolution.
