Summer Research Description: Heart disease is the leading cause of death in the United States. To date no therapeutics exist that target ischemia-reperfusion (IR) injury, which is a major contributor to heart failure. Hypoxia induced succinate has been implicated as a major source for IR induced reactive oxygen species production that is responsible for cardiac damage. TNNI3k is a cardiomyocyte specific kinase that our laboratory has determined to exacerbate ischemia-reperfusion injury in the heart. Substrate identification has led us to hypothesize that TNNI3k is intimately related to the regulation of succinate production during the ischemia state. Thus with its inhibition there will be a correlated decrease in the amount of ROS produced during IR. To investigate this, we will use an in-vitro model of hypoxia/reoxygenation with neonatal rat ventricular cardiomyocytes. Primary outcomes assessed will include western blot assessments of hypoxia induction and cell death, as well as colorimetric assay based detection of succinate. Overall, our data will provide a critical link between TNNI3K and IR induced cardiac damage.