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lüll Altered cAMP-mediated signalling and its role in the pathogenesis of dilated cardiomyopathy Movsesian MACardiovasc Res 2004[Jun]; 62 (3): 450-9Alterations 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.|Animals[MESH]|Cardiomyopathy, Dilated/*etiology/metabolism[MESH]|Cyclic AMP-Dependent Protein Kinases/genetics/metabolism[MESH]|Cyclic AMP/*metabolism[MESH]|Humans[MESH]|Mice[MESH]|Mice, Transgenic[MESH]|Models, Animal[MESH]|Phosphorylation[MESH]|Receptors, Adrenergic, beta/metabolism[MESH]|Signal Transduction/*physiology[MESH] |