| Literature DB >> 15098650 |
J van der Velden1, Z Papp, N M Boontje, R Zaremba, J W de Jong, P M L Janssen, G Hasenfuss, G J M Stienen.
Abstract
The increased Ca(2+)-responsiveness in end-stage human heart failure cannot be attributed to contractile protein isoform changes, but rather is the complex resultant of changes in degree of phosphorylation of VLC-2 and TnI. Despite the decreased basal level of VLC-2 phosphorylation the response to VLC-2 dephosphorylation is enhanced in failing myocytes, which might result from differences in endogenous phosphorylation of thin and thick filament proteins between donor and failing hearts. Taken together decreased VLC-2 phosphorylation in end-stage human heart failure might represent a compensatory process leading to an improvement of myocardial contractility by opposing the detrimental effects of increased Ca(2+)-responsiveness of force and impaired Ca(2+)-handling on diastolic function.Entities:
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Year: 2003 PMID： 15098650 DOI： 10.1007/978-1-4419-9029-7_1
Source DB: PubMed Journal: Adv Exp Med Biol ISSN： 0065-2598 Impact factor: 2.622