Inverse of coagulation. Plasminogen is the inactive zymogen, activated by tPA (endothelial, fibrin-targeted) or uPA (urokinase, broader). Plasmin cleaves fibrin → fibrin degradation products (D-dimer being the diagnostic marker). PAI-1 inhibits tPA/uPA; α2-antiplasmin inhibits free plasmin. Therapeutic thrombolysis (alteplase, tenecteplase, reteplase) for STEMI + acute ischemic stroke + massive PE works at the tPA step. Tranexamic acid (TXA) is the prototype antifibrinolytic — inhibits plasminogen lysine-binding to fibrin, blocking plasmin generation — used to reduce surgical/trauma/obstetric bleeding.
Organ Systems
immune-hematologic
cardiovascular
Pathway Steps
plasminogen → plasmin — via tPA (endothelial) or uPA (urokinase); fibrin-targeted. tPA (endothelial) and urokinase convert fibrin-bound plasminogen to plasmin, with fibrin itself acting as a cofactor that focuses fibrinolysis on the clot. Recombinant tPA (alteplase) is the thrombolytic for acute stroke/MI; PAI-1 and α2-antiplasmin restrain it.
plasmin → fibrin-degradation-products — via plasmin cleaves fibrin → D-dimer + FDPs. Plasmin digests cross-linked fibrin into D-dimer and other FDPs — D-dimer being the marker used to rule out VTE/DIC. Antifibrinolytics (tranexamic acid, aminocaproic acid) block plasmin(ogen) to reduce bleeding.