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Cardiovascular Research Advance Access originally published online on August 21, 2007
Cardiovascular Research 2008 77(2):334-343; doi:10.1093/cvr/cvm005
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2007. For Permissions please e-mail: journals.permissions@oxfordjournals.org

Heart mitochondria: gates of life and death

Åsa B. Gustafsson* and Roberta A. Gottlieb

BioScience Center San Diego State University 5500 Campanile Drive San Diego, CA 92182-4650, USA

* Corresponding author. Tel: +1 619 594 8977; fax: +1 619 594 8984. E-mail address: agustafs{at}sciences.sdsu.edu

Mitochondria are important generators of energy, providing ATP through oxidative phosphorylation. However, mitochondria also monitor complex information from the environment and intracellular milieu, including the presence or absence of growth factors, oxygen, reactive oxygen species, and DNA damage. Mitochondria have been implicated in the loss of cells in various cardiac pathologies, including ischaemia/reperfusion injury, cardiomyopathy, and congestive heart failure. The release of factors such as cytochrome c, Smac, Omi/Htr2A, and AIF from mitochondria serves to activate a highly complex and regulated cell death program. Furthermore, mitochondrial calcium overload might trigger opening of the mitochondrial permeability transition pore, causing uncoupling of oxidative phosphorylation, swelling of the mitochondria due to influx of water, and rupture of the mitochondrial outer membrane. In this review, we discuss the role of mitochondria in the control of cell death in cardiac myocytes.

KEYWORDS Apoptosis; Mitochondria; Myocytes; Necrosis; Reperfusion

Time for primary review: 29 days


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 Cardiovasc ResHome page
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