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Updated: Jun 10, 2026

Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents
Published on: July 3, 2013
Calmodulin kinase II, sarcoplasmic reticulum Ca2+ leak, and atrial fibrillation
Dobromir Dobrev1, Xander H T Wehrens
1Department of Pharmacology and Toxicology, Dresden University of Technology, Germany. dobrev@rcs.urz.tu-dresden.de
Abstract:
Although it is generally accepted that excitation-contraction coupling is defective in patients with atrial fibrillation, the underlying cellular mechanisms remain incompletely understood. Recent studies suggest that abnormal sarcoplasmic reticulum calcium "leak" via ryanodine receptors contributes to atrial arrhythmogenesis. Increased activity of the enzyme calmodulin kinase II (CaMKII) and, specifically, enhanced CaMKII phosphorylation of ryanodine receptors appear to play a critical role in the induction and perhaps maintenance of atrial fibrillation. In this review, we will summarize new insights into the role of enhanced CaMKII in sarcoplasmic reticulum calcium leak and atrial arrhythmogenesis during atrial fibrillation.
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