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Cardiovasc Res. 2011 May 1;90(2):234-42. doi: 10.1093/cvr/cvr015. Epub 2011 Jan 21.

Mitochondrial adaptations to physiological vs. pathological cardiac hypertrophy.

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  • 1Division of Endocrinology, Metabolism and Diabetes, and Program in Molecular Medicine, University of Utah School of Medicine, 15 North 2030 East, Bldg. 533, Rm. 3110B, Salt Lake City, UT 84112, USA. dale.abel@hmbg.utah.edu

Abstract

Cardiac hypertrophy is a stereotypic response of the heart to increased workload. The nature of the workload increase may vary depending on the stimulus (repetitive, chronic, pressure, or volume overload). If the heart fully adapts to the new loading condition, the hypertrophic response is considered physiological. If the hypertrophic response is associated with the ultimate development of contractile dysfunction and heart failure, the response is considered pathological. Although divergent signalling mechanisms may lead to these distinct patterns of hypertrophy, there is some overlap. Given the close relationship between workload and energy demand, any form of cardiac hypertrophy will impact the energy generation by mitochondria, which are the key organelles for cellular ATP production. Significant changes in the expression of nuclear and mitochondrially encoded transcripts that impact mitochondrial function as well as altered mitochondrial proteome composition and mitochondrial energetics have been described in various forms of cardiac hypertrophy. Here, we review mitochondrial alterations in pathological and physiological hypertrophy. We suggest that mitochondrial adaptations to pathological and physiological hypertrophy are distinct, and we shall review potential mechanisms that might account for these differences.

PMID:
21257612
[PubMed - indexed for MEDLINE]
PMCID:
PMC3115280
Free PMC Article
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