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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Fibrinolytic proteins linked to thrombotic and hemorrhagic disorders