Format

Send to

Choose Destination
See comment in PubMed Commons below
J Mol Cell Cardiol. 2011 Oct;51(4):479-84. doi: 10.1016/j.yjmcc.2010.10.020. Epub 2010 Oct 28.

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

Author information

  • 1Department of Chemical and Systems Biology, Stanford University School of Medicine, CCSR, Rm 3145A, 269 Campus Drive, Stanford, CA 94305-5174, USA.

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".

PMID:
21035454
PMCID:
PMC3135714
DOI:
10.1016/j.yjmcc.2010.10.020
[PubMed - indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science Icon for PubMed Central
    Loading ...
    Support Center