title: TGF-β and restenosis revisited: a Smad link.
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.
authors.affiliation: Department of Surgery, Division of Vascular Surgery, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, USA.
authors.forename: Pasithorn A
authors.initials: PA
authors.lastname: Suwanabol
authors.forename: K Craig
authors.initials: KC
authors.lastname: Kent
authors.forename: Bo
authors.initials: B
authors.lastname: Liu
mesh_terms: D000818:Animals; D023903:Coronary Restenosis / Q000503:physiopathology*; D004195:Disease Models, Animal; D006801:Humans; D051379:Mice; D018345:Mice, Knockout; D015398:Signal Transduction / Q000502:physiology; D051785:Smad Proteins / Q000502:physiology*; D016212:Transforming Growth Factor beta / Q000502:physiology*; D017539:Tunica Intima / Q000473:pathology / Q000503:physiopathology
chemical_list: D051785:Smad Proteins; D016212:Transforming Growth Factor beta