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Updated: Jun 8, 2026

Crystal Structure of the N-terminal Domain of Ryanodine Receptor from Plutella xylostella
Published on: November 30, 2018
The ryanodine receptor channel as a molecular motif in atrial fibrillation: pathophysiological and therapeutic
Dobromir Dobrev1, Niels Voigt, Xander H T Wehrens
1Division of Experimental Cardiology, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany.
Abstract:
Atrial fibrillation (AF) is the most common cardiac arrhythmia and is associated with substantial morbidity and mortality. It causes profound changes in sarcoplasmic reticulum (SR) Ca(2+) homeostasis, including ryanodine receptor channel dysfunction and diastolic SR Ca(2+) leak, which might contribute to both decreased contractile function and increased propensity to atrial arrhythmias. In this review, we will focus on the molecular basis of ryanodine receptor channel dysfunction and enhanced diastolic SR Ca(2+) leak in AF. The potential relevance of increased incidence of spontaneous SR Ca(2+) release for both AF induction and/or maintenance and the development of novel mechanism-based therapeutic approaches will be discussed.
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