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.
journal_name
Adv Exp Med Bioljournal_title
Advances in experimental medicine and biologyauthors
van der Velden J,Papp Z,Boontje NM,Zaremba R,de Jong JW,Janssen PM,Hasenfuss G,Stienen GJdoi
10.1007/978-1-4419-9029-7_1subject
Has Abstractpub_date
2003-01-01 00:00:00pages
3-15eissn
0065-2598issn
2214-8019journal_volume
538pub_type
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