IMR Press / FBS / Volume 1 / Issue 1 / DOI: 10.2741/S23

Frontiers in Bioscience-Scholar (FBS) is published by IMR Press from Volume 13 Issue 1 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

TGF-beta signaling in atherosclerosis and restenosis
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1 The George Washington University Medical Center, Department of Biochemistry and Molecular Biology, The Catharine Birch McCormick Genomics Center, and The Richard B. and Lynne V. Cheney Cardiovascular Institute, Washington, D.C. USA

*Author to whom correspondence should be addressed.

Academic Editor: Steven Dooley

Front. Biosci. (Schol Ed) 2009, 1(1), 236–245;
Published: 1 June 2009
(This article belongs to the Special Issue TGF-beta in fibroproliferative diseases)

Current theories suggest that atherosclerotic and restenotic lesions result from imbalances between systems that are proinflammatory/fibroproliferative versus the endogenous inhibitory systems that normally limit inflammation and vascular wound repair. Abnormalities in one of the major regulatory pathways, the transforming growth factor-ß (TGF-ß) system, has been characterized in both animal models and in human lesions and lesion-derived cells. TGF-ß signaling is capable of regulating many of the key aspects of atherosclerosis and restenosis: inflammation, chemotaxis, fibrosis, proliferation, and apoptosis. There are significant decreases in TGF-ß activity in patients with atherosclerosis, and equally important changes in the way cells respond to TGF-ß during atherogenesis. Evidence from multiple sources indicates that experimental modulation of TGF-ß activity, or TGF-ß responses, changes the course of atherosclerosis and intimal hyperplasia. Cells derived from human lesions produce adequate TGF-ß levels, but are resistant to the antiproliferative and apoptotic effects of TGF-ß. An evolving theory describes TGF-ß as a major orchestrator of the vascular repair process, with observable defects in its production, activation, and cellular responses during the atherosclerotic and restenotic processes.

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