My lab develops new tools to manipulate and assess cell metabolism and mitochondrial function in living systems. Our goal is to improve cellular resistance to environmental stresses and diseases through engineering metabolism.
Our laboratory is interested in identifying and targeting the key regulators of cell metabolism and mitochondrial function for the treatment of cardiovascular and metabolic diseases. We take multidisciplinary approaches to manipulate and interrogate the cellular metabolic network. For example, we perturb the metabolic network by altering its key element using bioengineered cells or animals and determine the metabolic and functional outcomes using multi-nuclear NMR spectroscopy and metabolomics. Using this strategy, we are studying the remodeling of cardiac metabolism during the development of pathological hypertrophy which is an abnormal growth of the heart that eventually leads to heart failure.
Another focus of our research is to develop mitochondria based cell protection. We recently revealed an important role of redox-sensitive protein acetylation in modulating mitochondrial protein interactome that in turn dictates cellular sensitivity to stress. We are now developing novel technologies with our collaborators, e.g. biosensors, quantitative proteomics and high throughput screening, to determine and target the nodal points of mitochondria-originated injury pathways.
2017 Fellow, American Institute of Medical and Biological Engineers (AIMBE)
2010 Distinguished Achievement Award of the American Heart Association Basic Science Council
2008 Elected to American Society of Clinical Investigation
2003-07 Established Investigator of the American Heart Association
2004 Young Investigator Award of the American Physiological Society
1999 Scholars in Medicine at the Harvard Medical School
1998 Scientist Development Award of the American Heart Association
1995 Upjohn Award for Young Investigators (Finalist), International Society for Heart Research
1988-1991 Award from Chinese State Committee of Education for Ph.D. studies in Denmark
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 PMCID:PMC3434870.
Karamanlidis G, Lee CF, Garcia-Menendez L, Kolwicz Jr. 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.
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 ?2-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. PMCID: PMC3971100.
Kolwicz SC Jr, Liu L, Goldberg IJ, Tian R. Enhancing Cardiac Triacylglycerol Metabolism Improves Recovery From Ischemic Stress. Diabetes. 2015 Aug;64(8):2817-27. doi: 10.2337/db14-1943. Epub 2015 Apr 9.
Wang W, Karamanlidis G, Tian R. Novel targets for mitochondrial medicine. Sci Transl Med. 2016 Feb 17;8(326):326rv3. doi: 10.1126/scitranslmed.aac7410. PubMed PMID: 26888432.
Lee CF, Chavez J, Garcia-Menendez L, Choi YS, Roe N, Chiao YA, Edgar J, Goo YA, Goodlett, Bruce J, Tian R. Normalization of NAD+ Redox Balance as a Therapy for Heart Failure. Circulation 2016, in press.