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University of Washington
School of Medicine
Box 358050
850 Republican Street
Brotman Building 453
Seattle, WA 98195-8050

Rong Tian, MD, PhD

Publications

Dr. Rong Tian

Department: Anesthesiology and Pain Medicine

Dr. Tian is the Director of the Mitochondria and Metabolism Center, located at the University of Washington's South Lake Union campus. She is also Co-director of the NMR Center, and Professor in the departments of Anesthesiology and Pain Medicine and Bioenineering.

Research in the Tian Laboratory focuses on the role of cell metabolism and mitochondrial function in the pathogenesis of human diseases. The laboratory uses multi-disciplinary approaches to identify novel regulatory mechanisms, perturb the metabolic networks, and interrogate metabolic fluxes and bioenergetics in a variety of model systems. Current studies concentrate on cardiac substrate metabolism, mitochondrial function and metabolic signaling by combining the powerful NMR techniques and metabolomics with ability to target the molecular regulatory mechanisms via genetic manipulation in animal models. Dr. Tian is also interested in bi-directional translational research between the bench and the bedside to elucidate the functional significance of altered cellular metabolism in ischemic heart disease, obesity, diabetes and heart failure.

Part of the Tian lab's current research examines the fundamental mechanisms linking altered cardiac metabolism and mitochondrial dysfunction to the pathogenesis of heart diseases. This line of work seeks to generate a basis for metabolic therapy for heart failure and cardiac lipotoxicity in obesity and diabetes. Studies in this direction extend to nutrient-mediated gene expression and programming of the cell during development, aging and disease conditions.

Another focus of the lab is to understand metabolic signaling in cardiovascular biology. They are interested in signaling mechanisms regulating cell metabolism under disease conditions as well as novel signaling functions of metabolites. For example, they were first to report that bioenergetic stress in pathological cardiac hypertrophy activates the AMP-activated protein kinase (AMPK), an energy sensor and master switch of metabolism. They subsequently generated mouse models with "gain-of-function" and "loss-of-function" of AMPK. Ongoing investigations in the lab address novel roles of AMPK in mitochondria biogenesis/function, cell growth and survival.