TGF-β and atherosclerosis in man

被引:118
作者
Grainger, David J. [1 ]
机构
[1] Univ Cambridge, Addenbrookes Hosp, Dept Med, Cambridge CB2 2QQ, England
关键词
blood vessel; T cell; autoimmunity; inflammation;
D O I
10.1016/j.cardiores.2007.02.022
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The transforming growth factor type-beta (TGF-beta) superfamily of ligands, receptors, binding proteins and ligand traps together plays a key role in the maintenance of normal blood vessel wall structure. Specific defects in genes encoding superfamily members have now been linked to a range of cardiovascular syndromes involving loss of healthy vessel architecture, including hypertension and aneurysm. However the contribution of TGF-beta to the development of atherosclerosis is simultaneously more subtle and more complex. TGF-beta ligands are produced by a range of different cell types, which also regulate release of the active cytokine that, in turn, signals through multiple receptor complexes on different cell types. Recent evidence suggests that the T cell may be both a key source of TGF-beta and a key target for its effects during atherogenesis, as in other chronic inflammatory disorders. Here we review the evidence for the role of TGF-beta in the human vasculature during atherogenesis, and evaluate the available data in the context of our knowledge from animal models of the disease. (c) 2007 European Society of Cardiology. Published by Elsevier B.V.
引用
收藏
页码:213 / 222
页数:10
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