Open AccessReactive Oxygen Species–Activated Ca/Calmodulin Kinase IIδ Is Required for Late I Na Augmentation Leading to Cellular Na and Ca Overload
Author(s) -
Stefan Wagner,
Hanna Maria Ruff,
Sarah L. Weber,
Sarah Bellmann,
Thomas Sowa,
Timo Schulte,
Mark E. Anderson,
Eleonora Grandi,
Donald M. Bers,
Johannes Backs,
Luiz Belardinelli,
Lars S. Maier
Publication year - 2011
Publication title -
circulation research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.899
H-Index - 336
eISSN - 1524-4571
pISSN - 0009-7330
DOI - 10.1161/circresaha.110.221911
Subject(s) - thapsigargin , chemistry , autophosphorylation , bapta , reactive oxygen species , myocyte , chelerythrine , angiotensin ii , endoplasmic reticulum , ryanodine receptor , calmodulin , calcium , medicine , intracellular , endocrinology , microbiology and biotechnology , biophysics , protein kinase a , biochemistry , protein kinase c , kinase , biology , receptor , organic chemistry
In heart failure Ca/calmodulin kinase (CaMK)II expression and reactive oxygen species (ROS) are increased. Both ROS and CaMKII can increase late I(Na) leading to intracellular Na accumulation and arrhythmias. It has been shown that ROS can activate CaMKII via oxidation.
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