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Cardiovascular Research 2004 64(2):198-207; doi:10.1016/j.cardiores.2004.06.030
© 2004 by European Society of Cardiology
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Copyright © 2004, European Society of Cardiology

Regulation of mitochondrial proliferation in the heart: power-plant failure contributes to cardiac failure in hypertrophy

Steffi Goffarta, Jürgen-Christoph von Kleist-Retzowa,b and Rudolf J. Wiesnera,*

aInstitute of Vegetative Physiology, University of Köln, Robert-Koch-Str. 39, 50931 Köln, Germany
bDepartment of Pediatrics, University of Köln, Joseph-Stelzmann-Str., 50924 Köln, Germany

* Corresponding author. Tel.: +49 221 478 3610; fax: +49 221 478 6965. Email address: rudolf.wiesner{at}uni-koeln.de

During hypertrophy, proliferation of mitochondria does not keep pace with the increasing energy demand of the heart. This probably contributes importantly to cardiac failure, together with other phenotypic changes occurring during the growth process. The problem may be even aggravated if defects of mitochondrial function itself and not external factors cause the hypertrophic process. Here we review the basic mechanisms controlling mitochondrial biogenesis, especially the pathways coordinating expression of nuclear encoded mitochondrial genes and the small mitochondrial genome, and how these mechanisms may be connected to the cardiomyocyte differentiation program during development as well as under physiological and pathological circumstances.

Abbreviations: CYTOX, cytochrome c oxidase • FAO, fatty acid oxidation • HCM, hypertrophy cardiomyopathy • mtDNA, mitochondrial DNA • NEM, nuclear encoded mitochondrial • RC, respiratory chain

We would like to dedicate this review to Radovan Zak (1931–1999), Professor at The University of Chicago Medical School, Associate Editor of Circulation Research and Journal of Molecular and Cellular Cardiology, who contributed much to our understanding of the basal mechanisms of cardiac hypertrophy.

Time for primary review 19 days


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