Copyright © 2006, European Society of Cardiology
The PGE2-Stat3 connection in cardiac hypertrophy
Institute of Pharmacology and Toxicology, University of Zurich, Winterthurerstrasse 190, CH-8057 Zurich, Switzerland
* Corresponding author. Tel.: +41 44 635 59 19; fax: +41 44 635 68 71. Email address: schaub@pharma.unizh.ch
Received 30 October 2006; revised 6 November 2006; accepted 9 November 2006
| The first 10% of the full text of this article appears below. |
See article by Frias et al. [6] (pages 57–65) in this issue.
 |
1. Stimulation of cardiomyocyte hypertrophy |
|---|
In vivo cardiac hypertrophy is a slow process in which the myocytes increase in size in response to increased workload due to either an increase in hemodynamic load or to a loss of functional myocytes. Although the mechanical load has long been recognized as the most powerful hypertrophic stimulus, its signal transmission from the cell surface to the nuclear transcription activities has largely remained elusive. Apart from the mechanical stress, the hypertrophic reaction is monitored by a large number of neurotransmitters, hormones, growth factors, and cell mediators that under normal conditions stay in balance within a limited range of variation [1]. However, under chronic mechanical overload, ischemic conditions, or late-onset genetic diseases, all of which may be accompanied by inflammation, the ensemble of
|
2. Stat3 here – who's knocking? |
|---|
|
3. The JAK/Stat pathway |
|---|
|
4. How may Stat3 be integrated into PGE2 signaling for cardiac hypertrophy? |
|---|
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  J.-L. Samuel, M. C. Schaub, M. Zaugg, M. Mamas, W. B. Dunn, and B. Swynghedauw Genomics in cardiac metabolism Cardiovasc Res, July 15, 2008; 79(2): 218 - 227. [Abstract] [Full Text] [PDF]
|
|