[HTML][HTML] Intracellular Na+ overload causes oxidation of CaMKII and leads to Ca2+ mishandling in isolated ventricular myocytes
S Viatchenko-Karpinski, D Kornyeyev, N El-Bizri… - Journal of Molecular and …, 2014 - Elsevier
S Viatchenko-Karpinski, D Kornyeyev, N El-Bizri, G Budas, P Fan, Z Jiang, J Yang…
Journal of Molecular and Cellular Cardiology, 2014•ElsevierAn increase of late Na+ current (I NaL) in cardiac myocytes can raise the cytosolic Na+
concentration and is associated with activation of Ca 2+/calmodulin-dependent protein
kinase II (CaMKII) and alterations of mitochondrial metabolism and Ca 2+ handling by
sarcoplasmic reticulum (SR). We tested the hypothesis that augmentation of I NaL can
increase mitochondrial reactive oxygen species (ROS) production and oxidation of CaMKII,
resulting in spontaneous SR Ca 2+ release and increased diastolic Ca 2+ in myocytes …
concentration and is associated with activation of Ca 2+/calmodulin-dependent protein
kinase II (CaMKII) and alterations of mitochondrial metabolism and Ca 2+ handling by
sarcoplasmic reticulum (SR). We tested the hypothesis that augmentation of I NaL can
increase mitochondrial reactive oxygen species (ROS) production and oxidation of CaMKII,
resulting in spontaneous SR Ca 2+ release and increased diastolic Ca 2+ in myocytes …
Abstract
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.
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