Skip Navigation

Cardiovascular Research 2007 74(2):207-212; doi:10.1016/j.cardiores.2006.07.012
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
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Leask, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Leask, A.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2006, European Society of Cardiology

TGFβ, cardiac fibroblasts, and the fibrotic response

Andrew Leask*

CIHR Group in Skeletal Development and Remodeling, Division of Oral Biology and Department of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, University of Western Ontario, Dental Sciences Building, London ON, Canada N6A 5C1

* Tel.: +1 519 661 2111x81102. Email address: Andrew.Leask{at}schulich.uwo.ca

The cytokine transforming growth factor β (TGFβ) is a major contributor to fibrogenic responses both in vitro and in vivo. TGFβ possesses many functions; thus, broadly targeting TGFβ signaling as an anti-fibrotic approach is anticipated to be problematic. Recent experiments, however, have begun to elucidate the signaling pathways through which TGFβ activates a fibrotic program. This review critically evaluates the evidence supporting TGFβ as a pro-fibrotic cytokine, with special attention to cardiac fibrosis, and suggests several possible points for selective drug intervention to combat chronic fibrotic disease.

KEYWORDS TGFbeta; Fibrosis; Endothelin; CTGF

Time for primary review 32 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
 Am. J. Physiol. Heart Circ. Physiol.Home page
Z. Ying, P. Yue, X. Xu, M. Zhong, Q. Sun, M. Mikolaj, A. Wang, R. D. Brook, L. C. Chen, and S. Rajagopalan
Air pollution and cardiac remodeling: a role for RhoA/Rho-kinase
Am J Physiol Heart Circ Physiol, May 1, 2009; 296(5): H1540 - H1550.
[Abstract] [Full Text] [PDF]

Home page
 Cardiovasc ResHome page
N. Hermida, B. Lopez, A. Gonzalez, J. Dotor, J. J. Lasarte, P. Sarobe, F. Borras-Cuesta, and J. Diez
A synthetic peptide from transforming growth factor-{beta}1 type III receptor prevents myocardial fibrosis in spontaneously hypertensive rats
Cardiovasc Res, February 15, 2009; 81(3): 601 - 609.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
U. Yokoyama, H. H. Patel, N. C. Lai, N. Aroonsakool, D. M. Roth, and P. A. Insel
The cyclic AMP effector Epac integrates pro- and anti-fibrotic signals
PNAS, April 29, 2008; 105(17): 6386 - 6391.
[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.