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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2007;27:1886.)
© 2007 American Heart Association, Inc.

Brief Reviews

Thrombospondins, Their Polymorphisms, and Cardiovascular Disease

Olga I. Stenina; Eric J. Topol; Edward F. Plow

From the Joseph J. Jacobs Center for Thrombosis and Vascular Biology and Department of Molecular Cardiology (O.I.S., E.F.P.), Cleveland Clinic, Ohio; and the Scripps Translational Science Institute and Division of Cardiovascular Diseases (E.J.T.), The Scripps Research Institute, La Jolla, Calif.

Correspondence to Edward F. Plow, PhD, Department of Molecular Cardiology/NB50, Cleveland Clinic Foundation/Lerner Research Institute, 9500 Euclid Avenue, Cleveland, OH 44195. E-mail plowe{at}ccf.org

The thrombospondins are a 5-member gene family that mediate cell-cell and cell-matrix interactions. The thrombospondins are either trimers or pentamers, and their functions depend on their abilities to interact with numerous extracellular ligands and cell surface receptors through the multiple domains that compose each subunit. Recent genetic studies have indicated associations of particular single nucleotide polymorphisms in 3 of the 5 thrombospondins with cardiovascular disease. This observation has stimulated efforts to understand how the thrombospondins influence cardiovascular pathology, to dissect how the individual polymorphisms alter the structure and function of the parent thrombospondin molecules, and to replicate the genetic data in different patient populations. This review seeks to summarize current information that has emerged on each of these fronts.

Thrombospondins are large, extracellular matrix glycoproteins which mediate cell-cell and cell-matrix interactions by binding numerous ligands and cell-surface receptors. Particular single nucleotide polymorphisms in 3 of the 5 thrombospondins have been associated with myocardial infarction. This review summarizes current information linking the thrombospondins and their polymorphisms to cardiovascular pathophysiology.

Key Words: single nucleotide polymorphisms • thrombospondin • myocardial infarction • endothelial cells

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