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TGF-β and Restenosis Revisited: A Smad Link

Journal

JOURNAL OF SURGICAL RESEARCH
Volume 167, Issue 2, Pages 287-297

Publisher

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.jss.2010.12.020

Keywords

restenosis; intimal hyperplasia; angioplasty; transforming growth factor-beta (TGF-beta); Smad

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Funding

  1. NIH [R01-HL068673, T32-HL07899]
  2. Society of University Surgeons

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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-beta), 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-beta-mediated vascular fibrosis. However, emerging data indicate that the role of TGF-b 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-b, making evident the need to redefine the precise role of this family of cytokines and its primary signaling pathway, Smad, in restenosis. Unraveling TGF-b signaling in intimal thickening and arterial remodeling will pave the way for a clearer understanding of restenosis and the development of innovative pharmacological therapies. Published by Elsevier Inc.

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