Skip Navigation

Cardiovascular Research 2006 71(2):208-215; doi:10.1016/j.cardiores.2006.03.016
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
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 Murdoch, C. E.
Right arrow Articles by Shah, A. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Murdoch, C. E.
Right arrow Articles by Shah, A. M.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2006, European Society of Cardiology

NADPH oxidase-dependent redox signalling in cardiac hypertrophy, remodelling and failure

Colin E. Murdoch, Min Zhang, Alison C. Cave and Ajay M. Shah*

Department of Cardiology, Cardiovascular Division, King's College London School of Medicine, Bessemer Road, London SE5 9PJ, United Kingdom

* Corresponding author. Tel.: +44 20 7346 3865; fax: +44 20 7346 4771. Email address: ajay.shah{at}kcl.ac.uk

Markers of increased oxidative stress are known to be elevated following acute myocardial infarction and in the context of chronic left ventricular hypertrophy or heart failure, and their levels may correlate with the degree of contractile dysfunction or cardiac deficit. An obvious pathological mechanism that may account for this correlation is the potential deleterious effects of increased oxidative stress through the induction of cellular dysfunction, energetic deficit or cell death. However, reactive oxygen species have several much more subtle effects in the remodelling or failing heart that involve specific redox-regulated modulation of signalling pathways and gene expression. Such redox-sensitive regulation appears to play important roles in the development of several components of the phenotype of the failing heart, for example cardiomyocyte hypertrophy, interstitial fibrosis and chamber remodelling. In this article, we review the evidence supporting the involvement of reactive oxygen species and redox signalling pathways in the development of cardiac hypertrophy and heart failure, with a particular focus on the NADPH oxidase family of superoxide-generating enzymes which appear to be especially important in redox signalling.

KEYWORDS NADPH oxidase; Heart; Hypertrophy; Heart failure; Oxidative stress; Reactive oxygen species; Redox signalling

Time for primary review 21 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
 J. Nutr.Home page
I. Papparella, G. Ceolotto, D. Montemurro, M. Antonello, S. Garbisa, G. Rossi, and A. Semplicini
Green Tea Attenuates Angiotensin II-Induced Cardiac Hypertrophy in Rats by Modulating Reactive Oxygen Species Production and the Src/Epidermal Growth Factor Receptor/Akt Signaling Pathway
J. Nutr., September 1, 2008; 138(9): 1596 - 1601.
[Abstract] [Full Text] [PDF]

Home page
 Circ. Res.Home page
D. Liu, L. Gao, S. K. Roy, K. G. Cornish, and I. H. Zucker
Role of Oxidant Stress on AT1 Receptor Expression in Neurons of Rabbits With Heart Failure and in Cultured Neurons
Circ. Res., July 18, 2008; 103(2): 186 - 193.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
T. Hayashi, C. Yamashita, C. Matsumoto, C.-J. Kwak, K. Fujii, T. Hirata, M. Miyamura, T. Mori, A. Ukimura, Y. Okada, et al.
Role of gp91phox-containing NADPH oxidase in left ventricular remodeling induced by intermittent hypoxic stress
Am J Physiol Heart Circ Physiol, May 1, 2008; 294(5): H2197 - H2203.
[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.