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Cardiovascular Research Advance Access originally published online on January 24, 2009
Cardiovascular Research 2009 82(2):229-239; doi:10.1093/cvr/cvp001
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that the original authorship is properly and fully attributed; the Journal, Learned Society and Oxford University Press are attributed as the original place of publication with correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions@oxfordjournals.org.

Protein kinase C in heart failure: a therapeutic target?

Suresh Selvaraj Palaniyandi1, Lihan Sun1, Julio Cesar Batista Ferreira1,2 and Daria Mochly-Rosen1,*

1 Department of Chemical and Systems Biology, Stanford University School of Medicine, CCSR, Rm 3145A, 269 Campus Drive, Stanford, CA 94305-5174, USA
2 School of Physical Education and Sport, University of São Paulo, SP 05508-900, Brazil

* Corresponding author. Tel: +1 650 725 7720; fax: +1 650 723 2253. E-mail address: mochly{at}stanford.edu

Heart failure (HF) afflicts about 5 million people and causes 300 000 deaths a year in the United States alone. An integral part of the pathogenesis of HF is cardiac remodelling, and the signalling events that regulate it are a subject of intense research. Cardiac remodelling is the sum of responses of the heart to causes of HF, such as ischaemia, myocardial infarction, volume and pressure overload, infection, inflammation, and mechanical injury. These responses, including cardiomyocyte hypertrophy, myocardial fibrosis, and inflammation, involve numerous cellular and structural changes and ultimately result in a progressive decline in cardiac performance. Pharmacological and genetic manipulation of cultured heart cells and animal models of HF and the analysis of cardiac samples from patients with HF are all used to identify the molecular and cellular mechanisms leading to the disease. Protein kinase C (PKC) isozymes, a family of serine–threonine protein kinase enzymes, were found to regulate a number of cardiac responses, including those associated with HF. In this review, we describe the PKC isozymes that play critical roles in specific aspects of cardiac remodelling and dysfunction in HF.

KEYWORDS Protein kinase C; Heart failure; Cardiac remodeling; Hypertrophy; Fibrosis and inflammation

Time for primary review: 21 days


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