Copyright © 2007, European Society of Cardiology
Understanding the role of transforming growth factor-β1 in intimal thickening after vascular injury
aDepartment of Internal Medicine, University of Western Ontario, Suite 1604, 1265 Richmond St. North, London, Ontario, Canada N6A 3M1
bCell Biology Laboratory, Baker Heart Research Institute, 75 Commercial Road, Melbourne, Victoria 3004, Australia
* Corresponding author. Tel.: +1 519 858 4971. Email address: razi.khan{at}gmail.com
Intimal thickening is the most important cause of in-stent restenosis. The pathology of intimal thickening is attributable to a local inflammatory response after vascular injury which results in the production of cytokines. Transforming growth factor-β1 (TGF-β1) is a profibrotic cytokine that is involved in the induction of intimal thickening. Up-regulation of TGF-β1 after arterial injury results in the activation of various downstream pathways which stimulate the proliferation and migration of vascular smooth muscle cells, as well as the production of local extracellular matrix proteins. Recent evidence suggests that antagonizing TGF-β1 activity with direct or indirect inhibitors may attenuate or prevent intimal thickening. Additionally, TGF-β1 synthesis, activation and downstream regulation may also serve as significant sources of treatment. This review attempts to show the role of TGF-β1 in the pathology of intimal thickening and underlines the importance of TGF-β1 as a target for therapy.
KEYWORDS Transforming growth factor-β1; Intimal thickening; Percutaneous coronary intervention; Vascular smooth muscle cell; Extracellular matrix; Transforming growth factor-β3; Tranilast
Time for primary review 18 days
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