Fibrinolyysi

Fibrinolyysi, known in English as fibrinolysis, is the physiological process that dissolves blood clots by proteolytically breaking down fibrin. It helps restore normal blood flow after vessel injury and prevents clots from persisting or growing longer than necessary.

Central to fibrinolysis is plasmin, an enzyme generated from its inactive precursor plasminogen. Plasmin is produced by activators such as tissue-type plasminogen activator (tPA) and urokinase-type plasminogen activator (uPA). Fibrin within a clot markedly enhances plasminogen activation, concentrating the reaction on the clot surface. Once formed, plasmin cleaves fibrin into soluble degradation products, including D-dimer, leading to clot breakdown.

Fibrinolysis is tightly regulated by inhibitors that limit plasmin generation and activity. Key regulators include plasminogen activator inhibitors (PAI-1 and PAI-2) and alpha-2-antiplasmin, which prevent excessive plasmin activity. The balance between coagulation and fibrinolysis depends on various signals, including thrombin generation and endothelial cues. Fibrin itself acts as a cofactor that localizes and accelerates plasmin generation on clots.

Clinically, fibrinolysis underpins thrombolytic therapy for acute ischemic events. Recombinant tissue plasminogen activator (alteplase) and related agents (such as tenecteplase) promote clot dissolution, sometimes in combination with imaging-guided decision making. Side effects include bleeding. Laboratory markers of fibrinolysis include elevated D-dimer and fibrin degradation products. Disorders of fibrinolysis can cause bleeding (hyperfibrinolysis) or thrombosis (hypofibrinolysis).