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J Surg Res. 2011 May 15;167(2):287-97. doi: 10.1016/j.jss.2010.12.020. Epub 2011 Jan 15.

TGF-β and restenosis revisited: a Smad link.

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  • 1Department of Surgery, Division of Vascular Surgery, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, USA.


Despite novel surgical therapies for the treatment of atherosclerosis, restenosis continues to be a significant impediment to the long-term success of vascular interventions. Transforming growth factor-beta (TGF-β), a family of cytokines found to be up-regulated at sites of arterial injury, has long been implicated in restenosis; a role that has largely been attributed to TGF-β-mediated vascular fibrosis. However, emerging data indicate that the role of TGF-β in intimal thickening and arterial remodeling, the critical components of restenosis, is complex and multidirectional. Recent advancements have clarified the basic signaling pathway of TGF-β, making evident the need to redefine the precise role of this family of cytokines and its primary signaling pathway, Smad, in restenosis. Unraveling TGF-β signaling in intimal thickening and arterial remodeling will pave the way for a clearer understanding of restenosis and the development of innovative pharmacological therapies.

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