On the hypothesis that the failing heart is energy starved: lessons learned from the metabolism of ATP and creatine

Curr Hypertens Rep. 2006 Dec;8(6):457-64. doi: 10.1007/s11906-006-0023-x.


Adenosine triphosphate (ATP) and phosphocreatine fall in the failing heart. New insights into the control of ATP synthesis, supply, and utilization, and how this changes in the failing heart, have emerged. In this article, we address four questions: What are the mechanisms explaining loss of ATP and creatine from the failing heart? What are the consequences of these changes? Can metabolism be manipulated to restore a normal ATP supply? Does increasing energy supply have physiologic consequences (ie, does it lead to improved contractile performance)? In part 1 we focus on ATP, in part 2 on creatine, and in part 3 on the relationship between creatine and purine metabolism and purine nucleotide signaling.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Adenosine Triphosphate / metabolism*
  • Animals
  • Creatine / metabolism*
  • Disease Progression
  • Energy Metabolism / physiology*
  • Heat-Shock Proteins / physiology
  • Humans
  • Membrane Transport Proteins / physiology
  • Myocardial Contraction / physiology
  • Myocardium / chemistry
  • Myocardium / metabolism
  • PPAR gamma / physiology
  • Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
  • Transcription Factors / physiology


  • Heat-Shock Proteins
  • Membrane Transport Proteins
  • PPAR gamma
  • PPARGC1A protein, human
  • Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
  • Transcription Factors
  • creatine transporter
  • Adenosine Triphosphate
  • Creatine