My research has focused on how defective regulation of ion channels can promote cardiac arrhythmias and heart failure, two of the most common causes of death in the developed world. Our work has demonstrated that abnormal regulation of intracellular calcium release channels known as ryanodine receptors promotes arrhythmogenesis in patients with atrial fibrillation or heart failure. Currently a major focus of the laboratory is on calmodulin-dependent kinase, and its role in modulating ryanodine receptors during the development of arrhythmias and heart failure. The laboratory is also focused on junctophilin, a protein expressed in junctional membrane complexes, in which calcium-induced calcium release occurs within muscle cells. Our studies have revealed that junctophilin is a critical component of the calcium release unit in cardiac cells, and that disruption of its function may lead to cardiomyopathy. By combining studies on human tissue samples and genetically engineered mouse models, we hope to improve our understanding of the molecular basis of cardiac electrophysiology and contractile function of the heart. Our goal is to translate a better understanding of cardiac ion channel function and calcium signaling into novel therapeutic strategies for cardiac arrhythmias disorders and heart failure.