Abstract
Cardiovascular disease (CVD), including arrhythmia, is the leading cause of death in New Zealand. Research into new targets for future drug development is extremely important to reduce the arrhythmogenic risk for CVD patients. The cardiac ryanodine receptor (RyR2) is a calcium (Ca2+) channel crucial for activating a normal cardiac contraction. In pathological circumstances, RyR2 triggers arrhythmia through uncontrolled Ca2+ release known as store-overload-induced-Ca2+-release (SOICR). SOICR can be increased due to phosphorylation of RyR2 by several proteins.
Recently, it has been identified that RyR2 can be phosphorylated by casein kinase II (CK2), suggesting controlling CK2 activity could also be a target for arrhythmias. The purpose of this pilot study is to investigate the effect CK2 inhibition on the generation of SOICR and arrhythmia.