Document Detail

Protein kinase Cα as a heart failure therapeutic target.
MedLine Citation:
PMID:  20937286     Owner:  NLM     Status:  MEDLINE    
Heart failure afflicts ~5 million people and causes ~300,000 deaths a year in the United States alone. Heart failure is defined as a deficiency in the ability of the heart to pump sufficient blood in response to systemic demands, which results in fatigue, dyspnea, and/or edema. Identifying new therapeutic targets is a major focus of current research in the field. We and others have identified critical roles for protein kinase C (PKC) family members in programming aspects of heart failure pathogenesis. More specifically, mechanistic data have emerged over the past 6-7 years that directly implicate PKCα, a conventional PKC family member, as a nodal regulator of heart failure propensity. Indeed, deletion of the PKCα gene in mice, or its inhibition in rodents with drugs or a dominant negative mutant and/or inhibitory peptide, has shown dramatic protective effects that antagonize the development of heart failure. This review will weigh all the evidence implicating PKCα as a novel therapeutic target to consider for the treatment of heart failure. This article is part of a special issue entitled "Key Signaling Molecules in Hypertrophy and Heart Failure."
Qinghang Liu; Jeffery D Molkentin
Related Documents :
18650976 - Beneficial effects of sauna bathing for heart failure patients.
11242286 - Failures of splenic nonoperative management: is the glass half empty or half full?
12793706 - Heart failure in the elderly.
25189216 - The challenges of success: maintaining access to high quality pci in the face of declin...
469446 - Treatment of heart block due to sarcoid heart disease.
22817626 - Controlled release of thymosin β4 from injected collagen-chitosan hydrogels promotes a...
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review     Date:  2010-10-16
Journal Detail:
Title:  Journal of molecular and cellular cardiology     Volume:  51     ISSN:  1095-8584     ISO Abbreviation:  J. Mol. Cell. Cardiol.     Publication Date:  2011 Oct 
Date Detail:
Created Date:  2011-09-19     Completed Date:  2012-01-06     Revised Date:  2014-09-22    
Medline Journal Info:
Nlm Unique ID:  0262322     Medline TA:  J Mol Cell Cardiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  474-8     Citation Subset:  IM    
Copyright Information:
Copyright © 2010 Elsevier Ltd. All rights reserved.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Drug Evaluation, Preclinical
Gene Expression
Heart Failure / drug therapy*,  enzymology
Mice, Knockout
Molecular Targeted Therapy*
Myocardial Contraction
Myocardium / enzymology
Protein Kinase C-alpha / antagonists & inhibitors,  genetics,  metabolism*
Protein Kinase Inhibitors / therapeutic use
Grant Support
R01 HL062927/HL/NHLBI NIH HHS; R01 HL062927-13/HL/NHLBI NIH HHS; R01 HL105924/HL/NHLBI NIH HHS; R01 HL105924-02/HL/NHLBI NIH HHS; R37 HL060562/HL/NHLBI NIH HHS; R37 HL060562-15/HL/NHLBI NIH HHS; //Howard Hughes Medical Institute
Reg. No./Substance:
0/Protein Kinase Inhibitors; EC Kinase C-alpha

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Calmodulin kinase II inhibition prevents arrhythmias in RyR2(R4496C+/-) mice with catecholaminergic ...
Next Document:  Dispersal effects on a discrete two-patch model for plant-insect interactions.