Physiology Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Physiology 20: 303-315, 2005; doi:10.1152/physiol.00020.2005
1548-9213/05 $8.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (30)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by O’Rourke, B.
Right arrow Articles by Aon, M. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by O’Rourke, B.
Right arrow Articles by Aon, M. A.
Physiology, Vol. 20, No. 5, 303-315, October 2005
© 2005 Int. Union Physiol. Sci./Am. Physiol. Soc.

REVIEW

Mitochondrial Ion Channels: Gatekeepers of Life and Death

Brian O’Rourke, Sonia Cortassa and Miguel A. Aon

Institute of Molecular Cardiobiology, Division of Cardiology, The Johns Hopkins University, Baltimore, Maryland

bor{at}jhmi.edu

Continuous generation of ATP by mitochondrial oxidative phosphorylation is essential to maintain function in mechanically active cells such as cardiomyocytes. Emerging evidence indicates that mitochondrial ion channels activated by reactive oxygen species can induce a mitochondrial "critical" state, which can scale to cause electrical and contractile dysfunction of the cardiac cell and, ultimately, the whole heart. Here we focus on how mitochondrial ion channels participate in life-and-death decisions of the cell and discuss the challenges ahead for translating recent findings into novel therapeutic applications.




This article has been cited by other articles:


Home page
 MutagenesisHome page
J. A. Lemon, C. D. Rollo, and D. R. Boreham
Elevated DNA damage in a mouse model of oxidative stress: impacts of ionizing radiation and a protective dietary supplement
Mutagenesis, November 1, 2008; 23(6): 473 - 482.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Gastrointest. Liver Physiol.Home page
I. B. Nicoud, C. D. Knox, C. M. Jones, C. D. Anderson, J. M. Pierce, A. E. Belous, T. M. Earl, and R. S. Chari
2-APB protects against liver ischemia-reperfusion injury by reducing cellular and mitochondrial calcium uptake
Am J Physiol Gastrointest Liver Physiol, September 1, 2007; 293(3): G623 - G630.
[Abstract] [Full Text] [PDF]

Home page
 Cancer Res.Home page
S. S. N. Kolar, R. Barhoumi, J. R. Lupton, and R. S. Chapkin
Docosahexaenoic Acid and Butyrate Synergistically Induce Colonocyte Apoptosis by Enhancing Mitochondrial Ca2+ Accumulation
Cancer Res., June 1, 2007; 67(11): 5561 - 5568.
[Abstract] [Full Text] [PDF]

Home page
 FASEB J.Home page
G. R. Budas, A. Sukhodub, D. R. Alessi, and A. Jovanovic
3'phosphoinositide-dependent kinase-1 is essential for ischemic preconditioning of the myocardium
FASEB J, December 1, 2006; 20(14): 2556 - 2558.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2005 by the Int. Union Physiol. Sci./Am. Physiol. Soc.