Skip Navigation


Cardiovascular Research Advance Access originally published online on August 27, 2009
Cardiovascular Research 2009 84(2):176-177; doi:10.1093/cvr/cvp297
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
84/2/176    most recent
cvp297v2
cvp297v1
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 Jankowski, M.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Jankowski, M.
Related Collections
Right arrowRelated Article
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.

GATA4, a new regulator of cardiac fibroblasts, is sensitive to natriuretic peptides

Marek Jankowski*

Centre de Recherche, Centre Hospitalier de l'Université de Montréal, 3850 St Urbain Street, Montreal, QC, Canada H2W 1T7

* Corresponding author. Tel: +1 514 890 8000; fax: +1 514 412 7204; E-mail address: marek.jankowski@umontreal.ca

This editorial refers to ‘Atrial natriuretic peptide suppresses endothelin gene expression and proliferation in cardiac fibroblasts through a GATA4-dependent mechanism’ by D.J. Glenn et al., pp. 209–217, this issue.

The first 10% of the full text of this article appears below.

Cardiac fibroblasts are the most prevalent cell type in the heart. These cells exert a critical role in regulating normal myocardial function and in adverse myocardial remodelling that occur with hypertension, myocardial infarction, and heart failure.1 In normal cardiac tissue, fibroblasts are found throughout the cardiac tissue in parallel to the prevailing direction of muscle fibres. In essence, every cardiac myocyte is therefore in direct contact with fibroblasts. Adverse myocardial remodelling includes enlargement of myocytes, proliferation of fibroblasts, and increased procollagen synthesis. Natriuretic peptides, including atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP), released from myocytes have been shown to act as autocine/paracrine factors that reduce . . . [Full Text of this Article]


   Funding
 

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

Related Article

Atrial natriuretic peptide suppresses endothelin gene expression and proliferation in cardiac fibroblasts through a GATA4-dependent mechanism
Denis J. Glenn, Dolkun Rahmutula, Minobu Nishimoto, Faquan Liang, and David G. Gardner
Cardiovasc Res 2009 84: 209-217. [Abstract] [Full Text] [PDF]