Contractile dysfunction and ventricular arrhythmias associated with heart 
failure have been attributed to aberrant sarcoplasmic reticulum (SR) Ca(2+) 
cycling. The study of junctin (JCN) and histidine-rich Ca(2+) binding protein 
(HRC) becomes of particular importance since these proteins have been shown to 
be critical regulators of Ca(2+) cycling. Specifically, JCN is a SR membrane 
protein, which is part of the SR Ca(2+) release quaternary structure that also 
includes the ryanodine receptor, triadin and calsequestrin. Functionally, JCN 
serves as a bridge between calsequestrin and the Ca(2+) release channel, 
ryanodine receptor. HRC is a SR luminal Ca(2+) binding protein known to 
associate with both triadin and the sarcoplasmic reticulum Ca(2+)-ATPase, and 
may thus mediate the crosstalk between SR Ca(2+) uptake and release. Indeed, 
evidence from genetic models of JCN and HRC indicate that they are important in 
cardiophysiology as alterations in these proteins affect SR Ca(2+) handling and 
cardiac function. In addition, downregulation of JCN and HRC may contribute to 
Ca(2+) cycling perturbations manifest in the failing heart, where their protein 
levels are significantly reduced. This review examines the roles of JCN and HRC 
in SR Ca(2+) cycling and their potential significance in heart failure.