Skip Navigation


Cardiovascular Research Advance Access originally published online on May 9, 2009
Cardiovascular Research 2009 83(1):3-4; doi:10.1093/cvr/cvp147
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
83/1/3    most recent
cvp147v2
cvp147v1
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 Gladka, M.
Right arrow Articles by da Costa Martins, P. A.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Gladka, M.
Right arrow Articles by da Costa Martins, P. A.
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.

Aquaporin 7: the glycerol aquaeductus in the heart

Monika Gladka1, Hamid el Azzouzi1,2, Leon J. De Windt1,2 and Paula A. da Costa Martins1,*

1 Department of Medical Physiology, Division of Heart and Lungs, University Medical Center Utrecht, Utrecht, The Netherlands
2 Hubrecht Institute and Interuniversity Cardiology Institute Netherlands, Royal Netherlands Academy of Sciences, Utrecht, The Netherlands

* Corresponding author. Tel: +31 30 253 8900; fax: +31 30 253 9036. E-mail address: p.a.dacostamartins@umcutrecht.nl

This editorial refers to ‘The heart requires glycerol as an energy substrate through aquaporin 7, a glycerol facilitator’ by T. Hibuse et al.,15 pp. 34–41, this issue.

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

Deprivation of available energy has been postulated to play a major role in the genesis of heart failure,1–3 and accumulating evidence points to the premise that changes in gene expression that alter energy metabolism weaken the heart muscle,4,5 reinforcing the logic of ameliorating energy substrates, and/or metabolism as a heart failure therapeutic. Reduced cardiac energy levels, in turn, influence a plethora of cardiac events, including free radical defense mechanisms which lower cardiomyocyte survivability,6 cardiac contractility,7 adverse remodelling and arrhythmogenic susceptibility.8

The heart is able to produce energy from a wide range of substrates and shifts continuously between sources, according to supply availability as controlled by exercise, nutritional status, or pathophysiological conditions. Therefore, the immediate cardiac capacity . . . [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

The heart requires glycerol as an energy substrate through aquaporin 7, a glycerol facilitator
Toshiyuki Hibuse, Norikazu Maeda, Hideaki Nakatsuji, Yoshihiro Tochino, Koichi Fujita, Shinji Kihara, Tohru Funahashi, and Iichiro Shimomura
Cardiovasc Res 2009 83: 34-41. [Abstract] [Full Text] [PDF]