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Cardiovascular Research 2004 62(3):450-459; doi:10.1016/j.cardiores.2004.01.035
© 2004 by European Society of Cardiology
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Copyright © 2004, European Society of Cardiology

Altered cAMP-mediated signalling and its role in the pathogenesis of dilated cardiomyopathy

Matthew A Movsesian*

Cardiology Section, VA Salt Lake City Health Care System, Departments of Internal Medicine (Cardiology) and Pharmacology, University of Utah, 500 Foothill Boulevard, Salt Lake City, UT 84148, USA

* Tel.: +1-801-582-1565x4156; fax: +1-801-584-2532. Email address: matthew.movsesian{at}hsc.utah.edu

Alterations in the level and function of proteins involved in cAMP-mediated signalling are important in the pathophysiology and treatment of dilated cardiomyopathy. What is unclear is the extent to which these alterations, which attenuate receptor-stimulated cAMP generation, contribute to the pathogenesis of dilated cardiomyopathy and the extent to which they constitute a beneficial compensatory response. Studies in animals involving overexpression and ablation of proteins or peptides involved in cAMP-mediated signalling have yielded disparate results that are difficult to reconcile with a simple hypothesis. Our ability to understand these differences is limited by the lack of information on how these different genetic manipulations affect the phosphorylation of individual substrates of protein kinase A (PK-A) through which cAMP signals are transduced. This is important in view of evidence that the phosphorylation of individual PK-A substrates can be regulated selectively in different intracellular compartments, and that the phosphorylation of some PK-A substrates is increased in dilated cardiomyopathy while the phosphorylation of others is reduced. Approaches that quantify changes in the phosphorylation of individual PK-A substrates in models of dilated cardiomyopathy will provide information that may allow a better understanding of the pathogenesis of the syndrome and a more rational approach to its treatment.

KEYWORDS Altered cAMP-mediated signalling; Dilated cardiomyopathy; Protein kinase A

Time for primary review 21 days


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