faculty

Rong Tian

rongtian@uw.edu

University of Washington, 

Cell Signaling & Cell/Environment Interactions

Developmental Biology, Stem Cells & Aging

Mitochondrial and Metabolic mechanisms of human diseases

Faculty Contact Information

Building: SLU North Building Room: N130 Phone: 206-543-8982 Alt Phone: 206-616-5672 http://depts.washington.edu/mmcslu/faculty/rong-tian-md-phd/

Lab Information

Accepting Students For:

Rotation, Autumn
Rotation, Spring
Rotation, Summer
Rotation, Winter
Permanent

Publications

Heart specific knockout of Ndufs4 ameliorates ischemia reperfusion injury.

Zhang H, Gong G, Wang P, Zhang Z, Kolwicz SC, Rabinovitch PS, Tian R, Wang W.

Journal of molecular and cellular cardiology. 2018; 123:38-45. NIHMSID: NIHMS990623

PubMed [journal]
PMID:
30165037
PMCID:
PMC6192835

Mitochondrial dysfunction in pathophysiology of heart failure.

Zhou B, Tian R.

The Journal of clinical investigation. 2018; 128(9):3716-3726.

PubMed [journal]
PMID:
30124471
PMCID:
PMC6118589

Glucose promotes cell growth by suppressing branched-chain amino acid degradation.

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.

Nature communications. 2018; 9(1):2935.

PubMed [journal]
PMID:
30050148
PMCID:
PMC6062555

NAD(H) in Mitochondrial Energy Transduction: Implications for Health and Disease

Walker MA, Tian R.

Current Opinion in Physiology. 2018 June; 3(Mitochondrial Biology):101-109.

My Bibliography [journal]

Raising NAD in Heart Failure: Time to Translate?

Walker MA, Tian R.

Circulation. 2018; 137(21):2274-2277. NIHMSID: NIHMS954031

PubMed [journal]
PMID:
29784680
PMCID:
PMC5967641

Research Summary

The Tian Laboratory focuses on the roles of cell metabolism and mitochondrial function in the pathogenesis of human diseases. Our research combines the high resolution NMR techniques and metabolomics with the ability to target molecular regulatory mechanisms via genetic manipulation in animal models. Current research topics include:
Mitochondrial mechanisms in stress response;
Metabolic reprogramming during the development and disease;
Regulation of pathological cardiac hypertrophy by substrate metabolism.