Regulation of mitochondrial proliferation in the heart: power-plant failure contributes to cardiac failure in hypertrophy.
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.
Institute of Vegetative Physiology, University of Köln, Robert-Koch-Str. 39, 50931 Köln, Germany.
Steffi
S
Goffart
Jürgen-Christoph
JC
von Kleist-Retzow
Rudolf J
RJ
Wiesner
D006332:Cardiomegaly / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology*; D004261:DNA Replication; D004272:DNA, Mitochondrial / Q000378:metabolism; D004734:Energy Metabolism; D005786:Gene Expression Regulation; D006801:Humans; D008929:Mitochondria, Heart / Q000378:metabolism / Q000473:pathology*
D004272:DNA, Mitochondrial