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Fibrinolytic proteins linked to thrombotic and hemorrhagic disorders

Fibrinolytic proteins linked to thrombotic and hemorrhagic disorders
Protein Physiologic function Production and metabolism Consequence of abnormal expression
Plasminogen Precursor of plasmin, which degrades fibrin Produced in the liver Deficiency leads to poor wound healing and formation of fibrin-rich pseudomembranes on mucosal surfaces, most notably the eyes (ligneous conjunctivitis)
tPA, uPA Convert plasminogen to plasmin Cleared by the liver Overexpression or impaired clearance due to liver disease can increase bleeding risk
Alpha-2-antiplasmin Inhibits fibrinolysis Produced in the liver Deficiency can increase bleeding risk
PAI-1 Inhibits fibrinolysis Produced in the liver, vascular cells, and other cells

Deficiency can increase bleeding risk

Overexpression can increase thrombosis risk
TAFI (also called CPB2) Inhibits fibrinolysis Produced in the liver Overexpression linked to thrombosis; acquired deficiency (resulting from liver disease) could produce hemorrhage
Refer to UpToDate for details of the fibrinolytic process.
CPB2: carboxypeptidase B2; PAI-1: plasminogen activator inhibitor-1; TAFI: thrombin activatable fibrinolysis inhibitor; tPA: tissue-type plasminogen activator; uPA: urinary-type plasminogen activator (urokinase).
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