Skip Navigation

Cardiovascular Research 2006 70(2):191-199; doi:10.1016/j.cardiores.2006.01.016
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 Di Lisa, F.
Right arrow Articles by Bernardi, P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Di Lisa, F.
Right arrow Articles by Bernardi, P.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2006, European Society of Cardiology

Mitochondria and ischemia–reperfusion injury of the heart: Fixing a hole

Fabio Di Lisaa,c,* and Paolo Bernardib,c

aDipartimento di Chimica Biologica, Universitá di Padova, Viale G. Colombo 3, 35121 Padova, Italy
bDipartimento di Scienze Biomediche Sperimentali, Universitá di Padova, Viale G. Colombo 3, 35121 Padova, Italy
cIstituto di Neuroscienze del CNR, Universitá di Padova, Viale G. Colombo 3, 35121 Padova, Italy

* Corresponding author. Dipartimento di Chimica Biologica, Universitá di Padova, Viale G. Colombo 3, 35121 Padova, Italy. Tel.: +39 49 8276132; fax: +39 49 8073310. Email address: dilisa{at}civ.bio.unipd.it

Ischemia and post-ischemic reperfusion cause a wide array of functional and structural alterations of mitochondria. Although mitochondrial impairment is recognized as pivotal in determining loss of viability, the causal relationships among the various processes involved is ill defined. Nevertheless, a wide consensus exists in attributing a crucial role to opening of the mitochondrial permeability transition pore (PTP). Strong support for this concept has recently been provided by the reduced infarct size observed in mice lacking cyclophilin D. This protein located within the mitochondrial matrix favours PTP opening by increasing its sensitivity to Ca2+ in a process that is antagonized by cyclosporin A. Genetic approaches have also been used to demonstrate that adenine nucleotide translocase is not an essential component of the PTP. Here, we discuss our current understanding of the structure and function of PTP in the context of heart injury caused by ischemia and reperfusion.

KEYWORDS Mitochondria; Permeability transition; Reactive oxygen species; Ischemia; Cell death

Time for primary review 20 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
 Ann. Thorac. Surg.Home page
B. G. Leshnower, S. Kanemoto, M. Matsubara, H. Sakamoto, R. Hinmon, J. H. Gorman III, and R. C. Gorman
Cyclosporine preserves mitochondrial morphology after myocardial ischemia/reperfusion independent of calcineurin inhibition.
Ann. Thorac. Surg., October 1, 2008; 86(4): 1286 - 1292.
[Abstract] [Full Text] [PDF]

Home page
 J. Pharmacol. Exp. Ther.Home page
F. N. Obame, C. Plin-Mercier, R. Assaly, R. Zini, J. L. Dubois-Rande, A. Berdeaux, and D. Morin
Cardioprotective Effect of Morphine and a Blocker of Glycogen Synthase Kinase 3{beta}, SB216763 [3-(2,4-Dichlorophenyl)-4(1-methyl-1H-indol-3-yl)-1H-pyrrole-2,5-dione], via Inhibition of the Mitochondrial Permeability Transition Pore
J. Pharmacol. Exp. Ther., July 1, 2008; 326(1): 252 - 258.
[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.