Intracellular Na+ overload causes oxidation of CaMKII and leads to Ca2+ mishandling in isolated ventricular myocytes.
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ABSTRACT:
SUBMITTER: Viatchenko-Karpinski S
PROVIDER: S-EPMC4250389 | biostudies-literature | 2014 Nov
REPOSITORIES: biostudies-literature
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Intracellular Na+ overload causes oxidation of CaMKII and leads to Ca2+ mishandling in isolated ventricular myocytes.
Viatchenko-Karpinski Serge S Kornyeyev Dmytro D El-Bizri Nesrine N Budas Grant G Fan Peidong P Jiang Zhan Z Yang Jin J Anderson Mark E ME Shryock John C JC Chang Ching-Pin CP Belardinelli Luiz L Yao Lina L
Journal of molecular and cellular cardiology 20140922
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 diasto ...[more]
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