Mitochondria in cardiac hypertrophy and heart failure

Mariana G. Rosca, Bernard Tandler, Charles L. Hoppel

Research output: Contribution to journalReview articlepeer-review

169 Scopus citations

Abstract

Heart failure (HF) frequently is the unfavorable outcome of pathological heart hypertrophy. In contrast to physiological cardiac hypertrophy, which occurs in response to exercise and leads to full adaptation of contractility to the increased wall stress, pathological hypertrophy occurs in response to volume or pressure overload, ultimately leading to contractile dysfunction and HF. Because cardiac hypertrophy impairs the relationship between ATP demand and production, mitochondrial bioenergetics must keep up with the cardiac hypertrophic phenotype. We review data regarding the mitochondrial proteomic and energetic remodeling in cardiac hypertrophy, as well as the temporal and causal relationships between mitochondrial failure to match the increased energy demand and progression to cardiac decompensation. We suggest that the maladaptive effect of sustained neuroendocrine signals on mitochondria leads to bioenergetic fading which contributes to the progression from cardiac hypertrophy to failure. This article is part of a Special Issue entitled "Focus on Cardiac Metabolism".

Original languageEnglish
Pages (from-to)31-41
Number of pages11
JournalJournal of Molecular and Cellular Cardiology
Volume55
Issue number1
DOIs
StatePublished - Feb 2013

Keywords

  • Cardiac hypertrophy
  • Heart failure
  • Mitochondria
  • Oxidative phosphorylation

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