Professor James Johnson, Visiting Professor of Integrated Physiology from The University of British Columbia - In vivo control of heart rate and cardiomyocyte metabolism by Ryr2-mediated calcium flux


Cardiac ryanodine receptors (RYR2) have been reported to be decreased in disease states, including diabetes and heart failure, and perhaps also as a consequence of aging. The goal of our studies is to unequivocally define the effect of losing 50% of the ryanodine receptor proteins in the heart to help answer several long-standing questions in the field. The first objective of was to determine whether having a full complement of ryanodine receptor channels is really important for setting heart rate and whether a partial reduction in these channels would, by itself, result in lethal arrhythmias. The second objective was to determine whether these ryanodine receptor channels play an important role in the organization of the heart muscle cells. The third objective was to find out whether a partial loss of ryanodine receptor channels alters the way heart cells store and use energy from fats versus carbohydrates. We are also interested to how the energy status of the heart cells controls whether the cells decide to commit ‘cell suicide’. Collectively, this new information will help us understand the exact causes of heart failure, diabetic heart disease and arrhythmia, and inform efforts to stop these diseases.