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Cardiovascular Research Advance Access first published online on November 30, 2007
This version [Accepted Manuscript] published online on December 19, 2007
Cardiovascular Research, doi:10.1093/cvr/cvm079
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Sarcomeric Dysfunction in Heart Failure

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

1 Laboratory for Physiology, Institute for Cardiovascular Research, VU University Medical Center, 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

Correspondence to: Jolanda van der Velden, PhD Laboratory for Physiology, VUmc van der Boechorststraat 7 1081 BT Amsterdam The Netherlands Phone. 31-20-4448123 Fax. 31-20-4448255 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


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R. J. Solaro and P. P. de Tombe
Review focus series: sarcomeric proteins as key elements in integrated control of cardiac function
Cardiovasc Res, March 1, 2008; 77(4): 616 - 618.
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