Skip Navigation



Cardiovascular Research Advance Access [Accepted Manuscript] published online on February 16, 2009
Cardiovascular Research, doi:10.1093/cvr/cvp063
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
83/2/226    most recent
cvp063v2
cvp063v1
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 Gomez, L.
Right arrow Articles by Ovize, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Gomez, L.
Right arrow Articles by Ovize, M.
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.

Inhibition of mitochondrial permeability transition pore opening: translation to patients

Ludovic Gomez1, Bo Li1, Nathan Mewton2, Ingrid Sanchez2, Christophe Piot3,4, Meier Elbaz5,6 and Michel Ovize1,2

1 Inserm U 886, Lyon, France
2 Hospices Civils de Lyon, Université Claude Bernard Lyon1, Lyon, France
3 Inserm U661, Montpellier, France
4 Hopital Arnaud de Villeneuve, Université de Montpellier I and II, Montpellier, France
5 Inserm U858, Toulouse, France
6 Hôpital Rangueil, University Paul Sabatier, Toulouse, France

Address for correspondence: Prof. Michel Ovize, Inserm U886 - Laboratoire de Physiologie Lyon-Nord, 8, avenue Rockefeller, 69373 Lyon, FRANCE, Phone: (+33)-4-78-77-70-74 Fax: (+33)-4-78-77-71-75 E-mail: Michel.ovize{at}recherche.univ-lyon1.fr

A large body of experimental evidence indicates that during an acute myocardial infarction, tissue injury occurring after reperfusion represents a significant amount of the whole, irreversible damage. It is now recognized that mitochondrial permeability transition pore opening plays a crucial role in this specific component of myocardial infarction. Ischemic postconditioning and cyclosporine A have been shown to dramatically reduce infarct size in many animal species. Recent proof-of-concept clinical trials support the idea that lethal myocardial reperfusion injury is also of significant importance in patients with ongoing acute myocardial infarction, and that targeting mitochondrial permeability transition by either PCI postconditioning or cyclosporine A can reduce infarct size and improve the recovery of contractile function after reperfusion. Large-scale trials are ongoing to address whether these new treatments may improve clinical outcome in reperfused acute myocardial infarction patients.

KEYWORDS ischemia; reperfusion; postconditioning; cyclosporine

Time for primary review: 33 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
 Cardiovasc ResHome page
H. M. Piper and D. Garcia-Dorado
Cardiac protection takes off
Cardiovasc Res, July 15, 2009; 83(2): 163 - 164.
[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.