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Rong Tian, MD, PhD

  • Director of Mitochondria and Metabolism Center

  • Professor of Anesthesiology & Pain Medicine, and Bioengineering

  • Adjunct Professor, Biochemistry and 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
  • Metabolic mechanisms of immunity, obesity and resilience to stress

Rong Tian describes her path to becoming a leader in Cardiovascular Science in the following article featured in Circulation Research:

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 of the American Heart Association Basic Science Council
2017           College of Fellows, American Institute for Medical and Biological Engineering
2017           Research Achievement Award of the International Society for Heart Research
2017           Bernard and Joan Marshall Distinguished Investigator, British Society for CV Research
2019           Berne Distinguished Lectureship of American Physiological Society




Selected Publications:


  1. Ritterhoff J, Young S, Villet O, Shao D, Neto FC, Bettcher LF, Hsu YA, Kolwicz Jr. SC, Raftery D, Tian R. Metabolic Remodeling Promotes Cardiac Hypertrophy by Directing Glucose to Aspartate Biosynthesis. Circ Res 2020 Jan 17; 126(2): 182-196. PMID: 31709908
  2. Tian R*, Colucci WS*, Arany Z, Bachschmid MM, Ballinger SW, Boudina S, Bruce JE, David W. Busija DW, Dikalov S, Dorn II GW, Galis ZS, Gottlieb GA, Kelly DP, Kitsis RN, Kohr MJ, Levy D, Lewandowski ED, McClung JM, Mochly-Rosen D, O’Brien KD, O’Rourke B, Park JY, Ping P, Sack MN, Sheu S-S, Shi Y, Shiva S, Wallace DC, PhD; Weiss RG, MD, Vernon HJ, Wong R, Schwartz-Longacre L. Unlocking the Secrets of Mitochondria in the Cardiovascular System: Path to a Cure in Heart Failure. Circulation 30 Sep 2019; 140:1205–1216
  3. Shao D, Villet O, Zhang Z, Choi SW, Yan J, Ritterhoff J, Gu H, Djukovic D, Christodoulou D, Kolwicz SC Jr, Raftery D, Tian R. Glucose promotes cell growth by suppressing branched-chain amino acid degradation. Nat Commun. 2018 Jul 26; 9(1):2935. doi: 10.1038/s 41467-018-05362-7. PMID: 30050148
  4. Zhou B, Tian R. Mitochondrial dysfunction in pathophysiology of heart failure. J Clin Invest. 2018 Aug 31; 128(9):3716-3726. doi: 10.1172/JCI120849. Epub 2018 Aug 20. PMID: 30124471
  5. Chavez JD, Lee CF, Caudal A, Tian R, Bruce Cross—linking and mass spectrometry: taking systems structural biology to heart. Cell Syst. 2018 Jan 24;6(1):136-141.e5. doi: 10.1016/j.cels.2017.10.017. Epub 2017 Nov 29. PMID:29199018
  6. Li T, Zhang Z, Kolwicz Jr. SC, Abell L, Roe ND, Kim M, Zhou B, Cao Y, Ritterhoff J, Gu H, Raftery D, Sun H, Tian R. Defective branched—chain amino acid (BCAA) catabolism disrupts glucose metabolism and sensitizes the heart to ischemia—reperfusion Cell Metab. 2017 Feb 7; 25(2):374—385. PMID: 28178567
  7. Lee CF, Chavez J, Garcia—Menendez L, Choi YS, Roe N, Chiao YA, Edgar J, Goo YA, Goodlett, Bruce J, Tian Normalization of NAD+ Redox Balance as a Therapy for Heart Failure. Circulation 2016 Sep 201; 34(12):883—94. doi: 10.1161/CIRCULATIONAHA.116.022495. Epub 2016 Aug 3. PMID:27489254
  8. Karamanlidis G, Lee CF, Garcia—Menendez L, Kolwicz SC, Suthammarak W, Gong G, Sedensky MM, Morgan PG, Wang W, Tian R. Mitochondria Complex I Deficiency Increases Protein Acetylation and Accelerates Heart Failure. Cell Metab. 2013 Aug 6;18(2):239—50. PMCID: PMC3779647.
  9. Kolwicz Jr. SC, Purohit S, Tian R. Cardiac Metabolism and its Interactions with Contraction, Growth, and Survival of Circ Res. 2013 Aug 16; 113(5):603—16. PMCID: PMC3845521.
  10. Kolwicz, 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 PMCID: PMC3434870.
  11. 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 Circulation. 2009; 119:2818—2828. Epub 2009 May 18. PMID:19451348 PMCID: PMC2765220.
  12. 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, Tian Aberrant activation of AMP—activated protein kinase remodels metabolic network in favor of cardiac glycogen storage. J Clin Invest. 2007 May; 117(5): 1432-9. Epub 2007 Apr 12. PMID:17431505 PMCID: PMC1847536.
  13. Luptak I, Balschi JA, Xing Y, Leone TC, Kelly DP, Tian Decreased contractile reserve in PPARα —null hearts can be rescued by increasing glucose transport and utilization. Circulation 2005; 112:2339—2346.
  14. Tian R, Musi N, D’Agostino J, Hirshman MF, Goodyear Increased AMP—activated protein kinase activity in rat hearts with pressure overload hypertrophy. Circulation 2001, 104:1664—1669.
  15. Liao R, Jain M, Cui L, D’Agostino J, Aiello F, Ngoy S, Mortensen RM, Tian Cardiac—specific overexpression of GLUT1 prevents the development of heart failure due to pressure—overload in mouse. Circulation 2002, 106, 2125— 2131.



Please use the link below to see all publications from Tian Lab: ending

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