Copyright © 2007, European Society of Cardiology
TGF-β and atherosclerosis in man
Department of Medicine, University of Cambridge, Box 157, Addenbrooke's Hospital Hills Road, Cambridge CB2 2QQ, United Kingdom
* Tel. :+44 1223 336812. Email address: djg15{at}cam.ac.uk, http://www.graingerlab.org.
The transforming growth factor type-β (TGF-β) 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-β to the development of atherosclerosis is simultaneously more subtle and more complex. TGF-β 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-β1 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-β in the human vasculature during atherogenesis, and evaluate the available data in the context of our knowledge from animal models of the disease.
KEYWORDS Blood vessel; T cell; Autoimmunity; Inflammation
Abbreviations: ECM, extracellular matrix • LDL, low density lipoprotein • SMC, smooth muscle cell • TGF-β, transforming growth factor type-β
Time for primary review 34 days
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