Myocardial AKT: the omnipresent nexus

Physiol Rev. 2011 Jul;91(3):1023-70. doi: 10.1152/physrev.00024.2010.

Abstract

One of the greatest examples of integrated signal transduction is revealed by examination of effects mediated by AKT kinase in myocardial biology. Positioned at the intersection of multiple afferent and efferent signals, AKT exemplifies a molecular sensing node that coordinates dynamic responses of the cell in literally every aspect of biological responses. The balanced and nuanced nature of homeostatic signaling is particularly essential within the myocardial context, where regulation of survival, energy production, contractility, and response to pathological stress all flow through the nexus of AKT activation or repression. Equally important, the loss of regulated AKT activity is primarily the cause or consequence of pathological conditions leading to remodeling of the heart and eventual decompensation. This review presents an overview compendium of the complex world of myocardial AKT biology gleaned from more than a decade of research. Summarization of the widespread influence that AKT exerts upon myocardial responses leaves no doubt that the participation of AKT in molecular signaling will need to be reckoned with as a seemingly omnipresent regulator of myocardial molecular biological responses.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Calcium Signaling / physiology
  • Cardiomyopathies / physiopathology
  • Cell Survival / physiology
  • Enzyme Activation
  • Humans
  • MicroRNAs / metabolism
  • Mitochondria / enzymology
  • Myocardial Contraction / physiology
  • Myocardium / enzymology*
  • Neovascularization, Physiologic / physiology
  • Protein Kinases / metabolism
  • Proto-Oncogene Proteins c-akt / metabolism*
  • Proto-Oncogene Proteins c-pim-1 / metabolism
  • Sex Characteristics
  • Signal Transduction / physiology

Substances

  • MicroRNAs
  • Protein Kinases
  • Proto-Oncogene Proteins c-akt
  • Proto-Oncogene Proteins c-pim-1