Rong Tian, MD, PhD

  • Director, Mitochondria and Metabolism Center
  • Co-director, NMR center
  • Professor, Anesthesiology and Pain Medicine, Bioengineering
  • Adjunct Professor, Biochemistry, Pathology

Research Interests

My research focuses on the molecular mechanisms regulating cell metabolism and energetics.  A long-term goal of my laboratory is to understand the role of mitochondria and metabolism in the pathogenesis of human diseases, in particular cardiovascular diseases.We have utilized molecular and genetic approaches to identify and perturb specific regulators in the key pathways of cardiac energy metabolism in mice and subsequently interrogated the physiological and biochemical responses in vivo during the development of heart failure using multi-nuclear NMR spectroscopy.  Our past work focused on the oxidative metabolism and mitochondrial ATP synthesis in heart failure using mouse models of altered glucose and fatty acid metabolism in the heart. Our recent work seeks to decipher the mechanistic links between impaired oxidative phosphorylation and mitochondria-triggered cell death during chronic stresses. Results of these studies identified an important role of cellular redox state in diseases caused by mitochondrial dysfunction including cardiovascular and neurological pathologies. 

The three key areas are:

  • Energy metabolism in cardiovascular diseases
  • Mitochondrial dysfunction and metabolic signaling
  • NMR spectroscopy and Imaging-guided spectroscopy

Honors and Awards

  • 2004        Young Investigator Award of the American Physiological Society
  • 2003-07   Established Investigator of the American Heart Association
  • 2008        Elected to American Society of Clinical Investigation
  • 2010        Distinguished Achievement Award, American Heart Association Basic Science Council

Selected Publications

  • Kim M, Hunter RW, Garcia-Menendez L, Gong G, Yang YY, Kolwicz SC Jr, Xu J, Wang W, Sakamoto K, Tian R. Mutation in the γ2-subunit of AMPK Stimulates Cardiomyocyte Proliferation and Hypertrophy Independent of Glycogen Storage. Circ Res. 2014 Mar 14;114(6):966-75. Epub 2014 Feb 6.
  • Karamanlidis G, Lee CF, Garcia-Menendez L, Kolwicz Jr. SC, Suthammarak W, Gong G, Sedensky MM, Morgan PG, Wang W, Tian R. Mitochondrial Complex I Deficiency Increases Protein Acetylation and Accelerates Heart Failure. Cell Metabolism. 2013 Aug 6;18(2):239-250.
  • Kolwicz Jr. SC, Olson DP, Marney LC, Garcia-Menendez L, Synovec RE, Tian R. Cardiac-specific deletion of acetyl CoA carboxylase 2 (ACC2) prevents metabolic remodeling during pressure-overload hypertrophy. Circ Res 2012, Aug 31; 111(6): 728-38. PMID: 22730442
  • Karamanlidis G, Nascimben L, Couper GS, Shekar PS, Tian R. Defective DNA replication impairs mitochondrial biogenesis In human failing hearts. Circ Res. 2010.
  • Yan J, Young ME, Cui L, Lopaschuk GD, Liao R, Tian R. Increased glucose uptake and oxidation in mouse hearts prevents high fatty acid oxidation but causes cardiac dysfunction in diet-induced obesity. Circulation 2009; 119:2818-2828.
  • Luptak I, Shen M, He H, Hirshman MF, Musi N, Goodyear LJ, Yan J, Wakimoto H, Morita H, Arad M , Seidman CE, Seidman JG, Ingwall JS ,Balschi JA, and Tian R. Aberrant activation of AMP-activated protein kinase remodels metabolic network in favor of cardiac glycogen storage. J Clin Invest. 2007; 117(5):1432-9.


Contact Information

Mitochondria and Metabolism Center
850 Republican Street, Room N130
University of Washington, Box 358057
Seattle, WA 98109-8057
Phone: 206-543-8982
Fax: 206-616-4819
Email: Rong Tian