Viatchenko-Karpinski, SergeKornyeyev, DmytroEl-Bizri, NesrineBudas, GrantFan, PeidongJiang, ZhanYang, JinAnderson, Mark E.Shryock, John C.Chang, Ching-PinBelardinelli, LuizYao, Lina2016-11-042016-11-042014-11Viatchenko-Karpinski, S., Kornyeyev, D., El-Bizri, N., Budas, G., Fan, P., Jiang, Z., … Yao, L. (2014). Intracellular Na+ Overload Causes Oxidation of CaMKII and leads to Ca2+ Mishandling in Isolated Ventricular Myocytes. Journal of Molecular and Cellular Cardiology, 0, 247–256. http://doi.org/10.1016/j.yjmcc.2014.09.0091095-8584https://hdl.handle.net/1805/11405An increase of late Na(+) current (INaL) 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 INaL 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. Increases of INaL and/or of the cytosolic Na(+) concentration led to mitochondrial ROS production and oxidation of CaMKII to cause dysregulation of Ca(2+) handling in rabbit cardiac myocytes.en-USAttribution-NonCommercial-NoDerivs 3.0 UnportedCalcium-Calmodulin-Dependent Protein Kinase Type 2metabolismMyocytes, CardiacenzymologySodiumArticle