Intracellular Na+ overload causes oxidation of CaMKII and leads to Ca2+ mishandling in isolated ventricular myocytes

Serge Viatchenko-Karpinski, Dmytro Kornyeyev, Nesrine El-Bizri, Grant Budas, Peidong Fan, Zhan Jiang, Jin Yang, Mark E. Anderson, John C. Shryock, Ching Pin Chang, Luiz Belardinelli, Lina Yao

Research output: Contribution to journalArticlepeer-review


An increase of late Na+ current (INaL) in cardiac myocytes can raise the cytosolic Na+ concentration and is associated with activation of Ca2+/calmodulin-dependent protein kinase II (CaMKII) and alterations of mitochondrial metabolism and Ca2+ handling by sarcoplasmic reticulum (SR). We tested the hypothesis that augmentation of INaL can increase mitochondrial reactive oxygen species (ROS) production and oxidation of CaMKII, resulting in spontaneous SR Ca2+ release and increased diastolic Ca2+ in myocytes. Increases of INaL and/or of the cytosolic Na+ concentration led to mitochondrial ROS production and oxidation of CaMKII to cause dysregulation of Ca2+ handling in rabbit cardiac myocytes.

Original languageEnglish (US)
Pages (from-to)247-256
Number of pages10
JournalJournal of Molecular and Cellular Cardiology
StatePublished - Nov 1 2014


  • ATX-II
  • CaMKII
  • Late sodium current
  • Mitochondria
  • ROS
  • RyRs

ASJC Scopus subject areas

  • Molecular Biology
  • Cardiology and Cardiovascular Medicine


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