Role of abnormal sarcoplasmic reticulum function in atrial fibrillation.

Atrial fibrillation (AF) is the most common cardiac arrhythmia, and is a cause of significant morbidity and mortality if left untreated. AF has been associated with profound changes in sarcoplasmic reticulum Ca(2+) homeostasis, which might contribute to both reduced contractile function and increased arrhythmogenesis in atria. Studies in human tissue samples and various animal models of AF have revealed changes in both expression levels and posttranslational modifications of key Ca(2+) handling proteins, which may contribute to arrhythmogenesis. In this review, we will focus on the molecular basis of alterations in sarcoplasmic reticulum Ca(2+) handling in AF and their potential therapeutic implications.