Key result
Increases of late Na+ current and cytosolic Na+ concentration led to mitochondrial ROS production and oxidation of CaMKII, causing dysregulation of Ca2+ handling in rabbit cardiac myocytes.
Augmentation of late Na+ current and cytosolic Na+ overload leads to mitochondrial ROS production and CaMKII oxidation, causing Ca2+ mishandling in ventricular myocytes.
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Suggests Na+-driven ROS-CaMKII pathway in myocyte Ca2+ mishandling; leaves open relevance to human HF or arrhythmias.
An 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.
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Viatchenko‐Karpinski et al. (2014) studied Isolated ventricular myocytes. Augmentation of late Na+ current (INaL) and intracellular Na+ overload was evaluated on Mitochondrial ROS production, oxidation of CaMKII, and dysregulation of Ca2+ handling. Increases of late Na+ current and cytosolic Na+ concentration led to mitochondrial ROS production and oxidation of CaMKII, causing dysregulation of Ca2+ handling in rabbit cardiac myocytes.
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