Hypophosphorylation of the Stiff N2B titin isoform raises cardiomyocyte resting tension in failing human myocardium.

@article{Borbly2009HypophosphorylationOT,
  title={Hypophosphorylation of the Stiff N2B titin isoform raises cardiomyocyte resting tension in failing human myocardium.},
  author={Attila Borb{\'e}ly and In{\^e}s Falc{\~a}o-Pires and Loek van Heerebeek and Nazha Hamdani and Istv{\'a}n {\'E}des and Cristina Gavina and Adelino F Leite-Moreira and Jean G. F. Bronzwaer and Zsuzsa Papp and Jolanda van der Velden and Ger J M Stienen and Walter Paulus},
  journal={Circulation research},
  year={2009},
  volume={104 6},
  pages={
          780-6
        }
}
High diastolic stiffness of failing myocardium results from interstitial fibrosis and elevated resting tension (F(passive)) of cardiomyocytes. A shift in titin isoform expression from N2BA to N2B isoform, lower overall phosphorylation of titin, and a shift in titin phosphorylation from N2B to N2BA isoform can raise F(passive) of cardiomyocytes. In left ventricular biopsies of heart failure (HF) patients, aortic stenosis (AS) patients, and controls (CON), we therefore related F(passive) of… CONTINUE READING

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