The multifunctional Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) 
regulates a rich variety of downstream targets in heart. Ca(2+) homeostatic 
proteins are important CaMKII targets that support myocardial 
excitation-contraction coupling. Under stress conditions, excessive CaMKII 
activity promotes heart failure and arrhythmias, in part through actions at 
Ca(2+) homeostatic proteins. Here, we briefly review the molecular and cellular 
physiology of CaMKII in myocardium.