TGF-beta signaling in atherosclerosis and restenosis

Front Biosci (Schol Ed). 2009 Jun 1;1:236-45. doi: 10.2741/s23.


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-beta (TGF-beta) system, has been characterized in both animal models and in human lesions and lesion-derived cells. TGF-beta 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-beta activity in patients with atherosclerosis, and equally important changes in the way cells respond to TGF-beta during atherogenesis. Evidence from multiple sources indicates that experimental modulation of TGF-beta activity, or TGF-beta responses, changes the course of atherosclerosis and intimal hyperplasia. Cells derived from human lesions produce adequate TGF-beta levels, but are resistant to the antiproliferative and apoptotic effects of TGF-beta. An evolving theory describes TGF-beta 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.

Publication types

  • Review

MeSH terms

  • Animals
  • Atherosclerosis / metabolism*
  • Atherosclerosis / pathology
  • Coronary Restenosis / metabolism*
  • Disease Models, Animal
  • Humans
  • Signal Transduction*
  • Transforming Growth Factor beta / metabolism*


  • Transforming Growth Factor beta