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Published Online
on June 14, 2007

Arteriosclerosis, Thrombosis, and Vascular Biology. 2007
Published online before print June 14, 2007, doi: 10.1161/ATVBAHA.107.141713
A more recent version of this article appeared on September 1, 2007
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Submitted on February 8, 2007
Accepted on May 16, 2007

Thrombospondins, Their Polymorphisms, and Cardiovascular Disease

Olga I. Stenina ; Eric J. Topol ; and 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.

* To whom correspondence should be addressed. E-mail: plowe{at}ccf.org.

Abstract--The thrombospondins are a 5-member gene family which mediate cell-cell and cell-matrix interactions. The thrombospondins are either trimers or pentameters, 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.


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




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