TGF-β and restenosis revisited: a Smad link

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

Abstract

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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Coronary Restenosis / physiopathology*
  • Disease Models, Animal
  • Humans
  • Mice
  • Mice, Knockout
  • Signal Transduction / physiology
  • Smad Proteins / physiology*
  • Transforming Growth Factor beta / physiology*
  • Tunica Intima / pathology
  • Tunica Intima / physiopathology

Substances

  • Smad Proteins
  • Transforming Growth Factor beta