A consistent theme of his work has been that mitochondrial dysfunction plays a key role in the mechanisms of arrhythmogenesis, contractile impairment and energetic abnormalities during the progression of heart failure and sudden cardiac death. Applying a systems biology approach, employing cardiac cell physiology, “omics”, and computational biology, his group has revealed the interplay between ion gradients, redox/ROS balance and energy supply, which, when disrupted, can trigger nonlinear mitochondrial responses that scale to cause global cardiac dysfunction and fatal arrhythmias. Development of therapies that improve the bioenergetic and redox functions of mitochondria is an area of increasing interest in the cardiovascular field, and his group has been a key contributor advancing these ideas. RESEARCH INTERESTS Heart Failure; Ischemia-Reperfusion; Arrythmias; Molecular manipulation of cardiac excitability; Mitochondria; Proteomics; Computational Biology; Oscillatory behavior of energy metabolism; Cardioprotection; Excitation-Contraction coupling in heart failure; Regulation of ion channels by energy metabolism in heart cells