Review |
From the Program in Molecular Cardiology and Department of Medicine (C.P., G.A.S., N.M., M.S.R.), Department of Pharmacology (C.P.), and Lineberger Comprehensive Cancer Center and Center for Thrombosis and Hemostasis (C.P., M.S.R.), University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
Correspondence to Cam Patterson, MD, University of North Carolina at Chapel Hill, 324 Burnett-Womack Building, Chapel Hill, NC 27599-7075. E-mail cpatters{at}med.unc.edu
AbstractThrombin is a serine protease that potently activates platelets and catalyzes the conversion of fibrinogen to fibrin. Thrombin also exerts direct effects on vascular cells, such as smooth muscle cells, via interactions with members of the protease-activated receptor family. Evidence in several animal models implicates thrombin-mediated signaling events in the response to injury that typifies vascular lesion formation in atherosclerosis and restenosis. In this review, we examine the activation of protease-activated receptors by thrombin, the downstream signaling events mediated by these receptors, and the physiological role of thrombin in vascular cells and vascular disease.
Key Words: atherosclerosis thrombin vascular biology
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