Cardiovascular Research Advance Access originally published online on August 7, 2008
Cardiovascular Research 2008 80(1):3-4; doi:10.1093/cvr/cvn213
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org
Lack of functional assembly in mitochondrial supercomplexes: a new insight into impaired mitochondrial function?
Grup de Metabolisme Energètic i Nutrició, Departament de Biologia Fonamental i Ciències de la Salut i Institut Universitari d'Investigació en Ciències de la Salut (IUNICS) de la Universitat de les Illes Balears, i CIBER Fisiopatología Obesidad y Nutrición (CB06/03) del Instituto de Salud Carlos III, Crta. Valldemossa km 7.5. E-07122-Palma de Mallorca, Spain
* Corresponding author. Tel: + 34 971 173 187; fax: + 34 971 173 184. E-mail address: paco.garcia-palmer@uib.es
This editorial refers to Cardiac mitochondria in heart failure: decrease in respirasomes and oxidative phosphorylation by Rosca et al.,1 pp. 30–39, this issue.
| The first 10% of the full text of this article appears below. |
A new mitochondrial disorder in heart failure that fits in the category of mitochondrial cytopathies is the exciting finding in the paper by Rosca et al.1 presented in this issue of Cardiovascular Research, which also explores a new insight into the functionality of mitochondria in the heart.
The function of heart muscle is highly dependent on the energy generated by mitochondria by oxidation of fatty acids and carbohydrates through the tricarboxylic acid cycle, which is the direct source of electrons for the respiratory electron chain where oxidative phosphorylation and associated ATP synthesis takes place. Defects in mitochondrial structure and
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Cardiovasc Res 2008 80: 30-39.