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

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

The Role of Diacylglycerol Acyltransferase (DGAT) 1 and 2 in Cardiac Metabolism and Function.

Roe ND, Handzlik MK, Li T, Tian R.

Scientific reports. 2018; 8(1):4983.

PubMed [journal]
PMID:
29563512
PMCID:
PMC5862879

Chemical Crosslinking Mass Spectrometry Analysis of Protein Conformations and Supercomplexes in Heart Tissue.

Chavez JD, Lee CF, Caudal A, Keller A, Tian R, Bruce JE.

Cell systems. 2018; 6(1):136-141.e5. NIHMSID: NIHMS922763

PubMed [journal]
PMID:
29199018
PMCID:
PMC5799023

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.