Abstract
Spontaneous release of Ca(2+) from the sarcoplasmic reticulum has emerged as a mechanism underlying triggered activity and cardiac arrhythmias. Recent studies suggest an important role for increased Ca(2+)/calmodulin-dependent protein kinase II (CaMKII)-mediated phosphorylation of ryanodine receptors (RyR2) in the induction of arrhythmias. This article briefly reviews the mechanisms underlying CaMKII regulation of RyR2 and discusses directions of current and future research.