Skip Navigation


Cardiovascular Research Advance Access first published online on May 15, 2009
This version [Corrected Proof] published online on June 4, 2009
Cardiovascular Research, doi:10.1093/cvr/cvp151
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
83/2/213    most recent
cvp151v2
cvp151v1
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 Zorov, D. B.
Right arrow Articles by Sollott, S. J.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Zorov, D. B.
Right arrow Articles by Sollott, S. J.
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.

Regulation and pharmacology of the mitochondrial permeability transition pore

Dmitry B. Zorov, Magdalena Juhaszova, Yael Yaniv, H. Bradley Nuss, Su Wang and Steven J. Sollott*

Laboratory of Cardiovascular Science, Gerontology Research Center, Box 13, Intramural Research Program, National Institute on Aging, NIH, 5600 Nathan Shock Drive, Baltimore, MD 21224-6825, USA

* Corresponding author. Tel: +1 410 558 8657; fax: +1 410 558 8150. E-mail address: sollotts{at}mail.nih.gov

The ‘mitochondrial permeability transition', characterized by a sudden induced change of the inner mitochondrial membrane permeability for water as well as for small substances (≤1.5 kDa), has been known for three decades. Research interest in the entity responsible for this phenomenon, the ‘mitochondrial permeability transition pore’ (mPTP), has dramatically increased after demonstration that it plays a key role in the life and death decision in cells. Therefore, a better understanding of this phenomenon and its regulation by environmental stresses, kinase signalling, and pharmacological intervention is vital. The characterization of the molecular identity of the mPTP will allow identification of possible pharmacological targets and assist in drug design for its precise regulation. However, despite extensive research efforts, at this point the pore-forming core component(s) of the mPTP remain unidentified. Pivotal new genetic evidence has shown that components once believed to be core elements of the mPTP (namely mitochondrial adenine nucleotide translocator and cyclophilin D) are instead only mPTP regulators (or in the case of voltage-dependent anion channels, probably entirely dispensable). This review provides an update on the current state of knowledge regarding the regulation of the mPTP.

KEYWORDS Adenine nucleotide translocator; Cyclophilin D; Mitochondrial voltage-dependent anion channel; Hexokinase; Creatine kinase; Mitochondrial peripheral benzodiazepine receptor; Bcl-2; Glycogen synthase kinase-3β

Time for primary review: 13 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.