More severe cellular phenotype in human idiopathic dilated cardiomyopathy compared to ischemic heart disease

• DOI: 10.1007/s10974-010-9231-8
• Publication Date: 2010-12-03T11:05:32Z
• Authors: Nazha Hamdani; Attila Borbély; Sophie P. G. R. V...; Viola Kooij; Wim Vrydag; Ruud Zaremba; Cris dos Remedios; Hans W. M. Niessen; Martin C. Michel; Walter J. Paulus; Ger J. M. Stienen; Jolanda van der V...
• Keywords: Phospholamban; Myofilament; Contractility; Dilated Cardiomyopathy

Activation of the β-adrenergic receptor (βAR) pathway is main mechanism heart to increase cardiac output via protein kinase A (PKA)-mediated phosphorylation cellular target proteins, and perturbations therein may contribute dysfunction in failure. In present study a comprehensive analysis was made mediators βAR pathway, myofilament properties structure patients with idiopathic (IDCM; n = 13) ischemic (ISHD; 10) cardiomyopathy comparison non-failing hearts (donor; for following parameters: density, G-coupled kinases 2 5, stimulatory inhibitory G-proteins, targets PKA, phosphatase 1, phospholamban, SERCA2a single myocyte contractility. All parameters exhibited expected alterations failure, but most them extent alteration greater IDCM than ISHD. Histological also revealed higher collagen compared Alterations are more pronounced ISHD reflect sequential changes composition function. Our data indicate that severe