Inhibition of Elevated Ca /Calmodulin-Dependent Protein Kinase II Improves Contractility in Human Failing Myocardium

نویسندگان

  • Samuel Sossalla
  • Nina Fluschnik
  • Hanna Schotola
  • Katharina R. Ort
  • Stefan Neef
  • Timo Schulte
  • Katrin Wittköpper
  • André Renner
  • Jan D. Schmitto
  • Jan Gummert
  • Ali El-Armouche
  • Gerd Hasenfuss
  • Lars S. Maier
چکیده

improved force frequency relationships in the presence of CaMKII inhibitors (KN-93 and AIP). Increased postrest twitches after CaMKII inhibition indicated an improved sarcoplasmic reticulum (SR) Ca loading. This was confirmed in isolated myocytes by a reduced SR Ca spark frequency and hence SR Ca leak, resulting in increased SR Ca load when inhibiting CaMKII. Ryanodine receptor type 2 phosphorylation at Ser2815, which is known to be phosphorylated by CaMKII thereby contributing to SR Ca leak, was found to be

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Clinical/Translational Research Inhibition of Elevated Ca /Calmodulin-Dependent Protein Kinase II Improves Contractility in Human Failing Myocardium

Rationale: Heart failure (HF) is known to be associated with increased Ca /calmodulin-dependent protein kinase (CaMK)II expression and activity. There is still controversial discussion about the functional role of CaMKII in HF. Moreover, CaMKII inhibition has never been investigated in human myocardium. Objective: We sought to investigate detailed CaMKII expression in end-stage failing human he...

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تاریخ انتشار 2010