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Recent advances in understanding endogenous fibrinolysis: implications for molecular-based treatment of vascular disorders

Published online by Cambridge University Press:  13 February 2004

Peter F. Bodary
Affiliation:
Division of Cardiology, University of Michigan Medical Center, 7315 MSRB III, 1150 W. Medical Center Drive, Ann Arbor, MI 49109-0644, USA.
Kevin J. Wickenheiser
Affiliation:
Division of Cardiology, University of Michigan Medical Center, 7315 MSRB III, 1150 W. Medical Center Drive, Ann Arbor, MI 49109-0644, USA.
Daniel T. Eitzman
Affiliation:
Division of Cardiology, University of Michigan Medical Center, 7315 MSRB III, 1150 W. Medical Center Drive, Ann Arbor, MI 49109-0644, USA.

Abstract

The fate of a forming thrombus is determined through the delicate balance between the coagulation cascade, favouring clot formation, and the fibrinolytic system, favouring clot lysis. These processes occur simultaneously, and enhancement of fibrinolysis has been shown to reduce occlusive thrombus formation in animal models. This review examines the roles of the major fibrinolytic factors involved in clot lysis. The regulation of plasmin activity by plasminogen activators, α-2-antiplasmin, plasminogen activator inhibitor 1, and thrombin-activatable fibrinolysis inhibitor, and their effects on thrombus formation in vivo are discussed. Since alterations in fibrinolytic capacity appear to affect thrombus formation in animal models, there is considerable interest in the pharmacological manipulation of fibrinolysis.

Type
Review Article
Copyright
© Cambridge University Press 2002

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