Mitochondrial energy metabolism in heart failure: a question of balance

J Clin Invest. 2005 Mar;115(3):547-55. doi: 10.1172/JCI24405.

Abstract

The mitochondrion serves a critical role as a platform for energy transduction, signaling, and cell death pathways relevant to common diseases of the myocardium such as heart failure. This review focuses on the molecular regulatory events and downstream effector pathways involved in mitochondrial energy metabolic derangements known to occur during the development of heart failure.

Publication types

  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • Cardiac Output, Low* / drug therapy
  • Cardiac Output, Low* / metabolism
  • Cardiac Output, Low* / physiopathology
  • Cardiomegaly / metabolism
  • Cardiomegaly / physiopathology
  • Cell Respiration / physiology
  • Energy Metabolism*
  • Heat-Shock Proteins / genetics
  • Heat-Shock Proteins / metabolism
  • Humans
  • Mitochondria / metabolism*
  • Myocardium / cytology
  • Myocardium / metabolism*
  • Myocardium / pathology
  • Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
  • Signal Transduction / physiology
  • Transcription Factors / genetics
  • Transcription Factors / metabolism
  • Transcription, Genetic

Substances

  • Heat-Shock Proteins
  • PPARGC1A protein, human
  • Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
  • Transcription Factors