βIIPKC and εPKC isozymes as potential pharmacological targets in cardiac hypertrophy and heart failure

J Mol Cell Cardiol. 2011 Oct;51(4):479-84. doi: 10.1016/j.yjmcc.2010.10.020. Epub 2010 Oct 28.

Abstract

Cardiac hypertrophy is a complex adaptive response to mechanical and neurohumoral stimuli and under continual stressor, it contributes to maladaptive responses, heart failure and death. Protein kinase C (PKC) and several other kinases play a role in the maladaptative cardiac responses, including cardiomyocyte hypertrophy, myocardial fibrosis and inflammation. Identifying specific therapies that regulate these kinases is a major focus of current research. PKC, a family of serine/threonine kinases, has emerged as potential mediators of hypertrophic stimuli associated with neurohumoral hyperactivity in heart failure. In this review, we describe the role of PKC isozymes that is involved in cardiac hypertrophy and heart failure. This article is part of a special issue entitled "Key Signaling Molecules in Hypertrophy and Heart Failure".

Publication types

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

MeSH terms

  • Animals
  • Cardiomegaly / drug therapy*
  • Cardiomegaly / enzymology
  • Heart Failure / drug therapy*
  • Heart Failure / enzymology
  • Humans
  • Isoenzymes / metabolism
  • Molecular Targeted Therapy
  • Myocardium / enzymology*
  • Protein Kinase C / metabolism*
  • Protein Kinase C beta
  • Protein Kinase C-epsilon / metabolism*
  • Protein Kinase Inhibitors / therapeutic use

Substances

  • Isoenzymes
  • Protein Kinase Inhibitors
  • Protein Kinase C
  • Protein Kinase C beta
  • Protein Kinase C-epsilon