Lay summary
A heart attack, otherwise known as a myocardial infarction, is the second leading cause of death in NZ. Those who survive suffer from arrhythmias and heart failure. Unfortunately, there are limited treatment options available for these patients. Diabetes exacerbates these outcomes with diabetic patients experiencing greater mortality and morbidity following a myocardial infarction. Arrhythmias and heart failure are both caused by ‘calcium leak’ through a protein known as the cardiac ryanodine receptor (RyR2). We have recently found that calcium leak increases when RyR2 phosphorylation by casein kinase 2 (CK2) decreases. CK2 activity is reduced during and after a myocardial infarction, and in diabetes and heart failure. Therefore, this project aims to determine if maintaining the phosphorylation of RyR2 by CK2 can prevent calcium leak, arrhythmias and heart failure in diabetes and following a myocardial infarction. In doing so it will identify a new target for treating arrhythmias and heart failure.