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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