Skip Navigation

Cardiovascular Research 2007 74(2):223-234; doi:10.1016/j.cardiores.2007.02.012
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Khan, R.
Right arrow Articles by Bobik, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Khan, R.
Right arrow Articles by Bobik, A.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2007, European Society of Cardiology

Understanding the role of transforming growth factor-β1 in intimal thickening after vascular injury

Razi Khana,*, Alex Agrotisb and Alex Bobikb

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


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Cardiovasc ResHome page
C. Rodriguez, J. Martinez-Gonzalez, B. Raposo, J. F. Alcudia, A. Guadall, and L. Badimon
Regulation of lysyl oxidase in vascular cells: lysyl oxidase as a new player in cardiovascular diseases
Cardiovasc Res, July 1, 2008; 79(1): 7 - 13.
[Abstract] [Full Text] [PDF]

Home page
 Arterioscler. Thromb. Vasc. Bio.Home page
K. Fu, M. J. Corbley, L. Sun, J. E. Friedman, F. Shan, J. L. Papadatos, D. Costa, F. Lutterodt, H. Sweigard, S. Bowes, et al.
SM16, an Orally Active TGF-{beta} Type I Receptor Inhibitor Prevents Myofibroblast Induction and Vascular Fibrosis in the Rat Carotid Injury Model
Arterioscler. Thromb. Vasc. Biol., April 1, 2008; 28(4): 665 - 671.
[Abstract] [Full Text] [PDF]


Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.