TGF-β and Restenosis Revisited: A Smad Link

被引:50
|
作者
Suwanabol, Pasithorn A. [1 ]
Kent, K. Craig [1 ]
Liu, Bo [1 ]
机构
[1] Univ Wisconsin, Dept Surg, Sch Med & Publ Hlth, Div Vasc Surg, Madison, WI 53705 USA
关键词
restenosis; intimal hyperplasia; angioplasty; transforming growth factor-beta (TGF-beta); Smad; GROWTH-FACTOR-BETA; SMOOTH-MUSCLE-CELLS; MEDIATED GENE-TRANSFER; TRANSFORMING GROWTH-FACTOR-BETA-1; TRANSCRIPTIONAL ACTIVATION; CORONARY ANGIOPLASTY; II RECEPTOR; DIABETIC-NEPHROPATHY; NEOINTIMAL FORMATION; TARGETED DISRUPTION;
D O I
10.1016/j.jss.2010.12.020
中图分类号
R61 [外科手术学];
学科分类号
摘要
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.
引用
收藏
页码:287 / 297
页数:11
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