Abstract
Calcium/calmodulin-dependent kinase II (CaMKII) holds a nodal position in cardiac signalling. Various activation mechanisms suggest CaMKII may act as a monitor of cellular metabolism, integrating this information to multiple downstream pathways to maintain homeostasis. However, this integral role becomes a liability during times of cellular stress when CaMKII becomes chronically overactivated, contributing to pathology. Therapeutic targeting of pathological outcomes will require a more thorough understanding of the intricacies of CaMKII signalling.