In the past few years, my research has been focused on understanding the role of mitochondrial autophagy and perturbations in mitochondrial morphology, dynamics and function in heart failure. My most recent work focuses on the role of the FOXO3a–BNIP3 axis in altering endoplasmic reticulum–mitochondrial calcium homeostasis and its consequences on mitochondrial dynamics and function as well as calcium cycling in heart failure. The FOXO3a–BNIP3 pathway is activated in animal models of pressure-overload-induced heart failure and in human systolic heart failure and contributes to mitochondrial dysfunction, myocardial remodeling and systolic dysfunction. Targeting (inhibition) the FOXO3a–BNIP3 pathway via gene therapy, in small animal models of heart failure, improved mitochondrial function and myocardial contractility and reversed myocardial remodeling. We would like to develop strategies inhibiting this pathway as a potential therapeutic strategy for patients with remodeled left ventricle and decreased systolic function.