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lüll TGF-beta and restenosis revisited: a Smad link Suwanabol PA; Kent KC; Liu BJ Surg Res 2011[May]; 167 (2): 287-97Despite 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-beta 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-beta, making evident the need to redefine the precise role of this family of cytokines and its primary signaling pathway, Smad, in restenosis. Unraveling TGF-beta signaling in intimal thickening and arterial remodeling will pave the way for a clearer understanding of restenosis and the development of innovative pharmacological therapies.|Animals[MESH]|Coronary Restenosis/*physiopathology[MESH]|Disease Models, Animal[MESH]|Humans[MESH]|Mice[MESH]|Mice, Knockout[MESH]|Signal Transduction/physiology[MESH]|Smad Proteins/*physiology[MESH]|Transforming Growth Factor beta/*physiology[MESH]|Tunica Intima/pathology/physiopathology[MESH] |