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. 2014 Mar 4;5:30. doi: 10.3389/fphar.2014.00030

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Copyright © 2014 Heijman, Voigt, Wehrens and Dobrev.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Atrial fibrillation (AF)-related mechanisms promoting CaMKII activation. AF-promoting conditions and/or AF itself can activate CaMKII via high atrial rates, oxidative stress, sympathetic hyperactivity, and hyperglycaemia, resulting in post-translational modifications (phosphorylation, oxidation, nitrosylation and glycosylation) of various residues in the regulatory domain of CaMKII. In addition, AF is associated with an increased total expression of the CaMKII holoenzyme. See text for details.