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Cardiovascular Research Advance Access originally published online on November 30, 2007
Cardiovascular Research 2008 77(4):649-658; doi:10.1093/cvr/cvm079
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2007. For permissions please email: journals.permissions@oxfordjournals.org

Sarcomeric dysfunction in heart failure

Nazha Hamdani1, Viola Kooij1, Sabine van Dijk1, Daphne Merkus2, Walter J. Paulus1, Cris dos Remedios3, Dirk J. Duncker2, Ger J.M. Stienen1 and Jolanda van der Velden1,*

1 Laboratory for Physiology, Institute for Cardiovascular Research, VU University Medical Center, van der Boechorststraat 7, 1081 BT Amsterdam, The Netherlands
2 Experimental Cardiology, Thoraxcenter, Cardiovascular Research School COEUR, Erasmus MC, University Medical Center Rotterdam, Rotterdam, The Netherlands
3 Muscle Research Unit, Institute for Biomedical Research, The University of Sydney, Sydney, Australia

* Corresponding author. Tel: + 31 20 4448123; fax: +31 20 4448255. E-mail address: j.vandervelden{at}vumc.nl

Sarcomeric dysfunction plays a central role in reduced cardiac pump function in heart failure. This review focuses on the alterations in sarcomeric proteins in diseased myocardium that range from altered isoform expression to post-translational protein changes such as proteolysis and phosphorylation. Recent studies in animal models of heart failure and human failing myocardium converge and indicate that sarcomeric dysfunction, including altered maximum force development, Ca2+ sensitivity, and increased passive stiffness, largely originates from altered protein phosphorylation, caused by neurohumoral-induced alterations in the kinase–phosphatase balance inside the cardiomyocytes. Novel therapies, which specifically target phosphorylation sites within sarcomeric proteins or the kinases and phosphatases involved, might improve cardiac function in heart failure.

KEYWORDS Sarcomere; Cardiomyocyte; Contractility; Heart failure

Time for primary review: 27 days


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