Targeting Mitochondrial Function in Heart Failure

The cardiac mitochondria are the power-houses of the cell and provide energy (ATP) to meet the physiologic demands of the heart. The by-product of energy generation is reactive oxygen species (ROS) production. We hypothesized that the heightened energy needs of the heart with complex CHD, coupled with excessive ROS production could damage the mitochondria, impairing their function, limiting energy generation and ultimately contributing to the heart failure phenotype. Our lab assesses mitochondrial function in patient samples using transmission electron microscopy, discovery proteomics, FACS, Seahorse and Oroboros assays to understand the mechanisms underlying mitochondrial dysfunction and to develop therapeutic targets with the goal of slowing or preventing heart failure progression.