Tian, Rong

Our laboratory is interested in the molecular mechanisms regulating mitochondrial function and cardiac metabolism. We perturb the metabolic network by altering its key element using genetics approaches and determine the metabolic and functional outcomes using biochemical measurements in combination with multi-nuclear NMR spectroscopy, MRI-guided metabolic imaging and metabolomics. We also create disease models and test the role of a specific metabolic alteration in the pathogenesis and progression of heart disease such as cardiac hypertrophy or diabetic cardiomyopathy. To this end, we are particularly interested in the dual role of mitochondria as a power plant and a death engine, and hope to identify nodal points for mitochondria-based cardioprotection that sustains oxidative metabolism and prevents cell death. A related effort is to understand the signaling mechanisms that regulate cellular metabolism in normal and disease conditions. For example, the AMPK pathway is highly sensitive to cellular energy status and activation of AMPK cascade regulates multiple aspects of cell metabolism and growth. We were the first to identify the hypertrophied heart as a chronic model in which AMPK was activated by impaired myocardial energetic. We are studying the biological role of AMPK in the heart utilizing gain-of-function and loss-of function approaches in both cellular and whole animal models.