The process of lysing the fibrin clot is called fibrinolysis. The pro-enzyme plasminogen is activated into plasmin, which cleaves the fibrin into smaller fragments. For the activation of plasminogen into active plasmin, tissue plasminogen activator (tPA) is needed. This reaction can be inhibited by TAFIa (Thrombin Activatable Fibrinolysis Inhibitor) which removes the lysins from the fibrin clot which are involved in the binding of plasminogen. TAFIa
is a carboxypeptidase formed from TAFI by thrombin. tPA is released from the endothelium. Plasminogen can also be activated via a still poorly understood mechanism which involves factor XII.
The fibrinolytic cascade is regulated by two inhibitors, α2-antiplasmin, an inhibitor of plasmin which circulates in the blood, and the plasminogen activator inhibitor (PAI-1), which inhibits tPA and is produced by endothelial cells.
In contrast to anticoagulation, fibrinolysis takes effect in:
Extra info: Fortunately for those patients suffering from an acute myocardial infarction, stimulation of the fibrinolytic process can take place within 4 to 24 hours after the infusion of a thrombolytic agent.