Qiang Shi Ph.D.
Visiting Scientist — Division of Systems Biology
Qiang Shi, Ph.D.
(870) 543-7121
NCTRResearch@fda.hhs.gov
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About | Publications | Lab Members
Background
Dr. Qiang Shi obtained a Ph.D. in pharmacology from Zhejiang University (China). His Ph.D. dissertation was on mouse liver protein modifications in drug induced liver injury (DILI). He completed his postdoctoral training in DILI at FDA’s National Center for Toxicological Research (NCTR) between 2007 and 2010, when he was then converted to a visiting scientist. Dr. Shi received the "FDA Outstanding Junior Investigator Award" in 2011, the FDA "Outstanding Intercenter Scientific Collaboration Award (Group)" in 2011 and 2016, and the FDA “Group Recognition Award” in 2021.
Research Interests
Dr. Shi’s main research focus is mechanisms and biomarkers for DILI. He has more than 15 years of experience in the culture of primary hepatocytes from multiple species with a mechanistic focus on drug-induced mitochondrial damage and metabolism-mediated hepatocyte injury. For biomarker studies, he uses in vitro systems and human clinical samples to explore novel translational DILI biomarkers, focusing on circulating micro-ribonucleic acids (microRNAs) in urine and blood. He has published more than 30 peer reviewed manuscripts on DILI. Dr. Shi’s most recent work involves the study of DILI induced by FDA-approved small-molecule kinase inhibitors and the use of liver-on-a-chip for liver adaptation in response to DILI. Long-term research goals include:
- Developing non-invasive translational biomarkers to predict DILI susceptibility, regeneration, and severity.
- Exploring alternative models, particularly in vitro models, to aid in the prediction of a chemical’s DILI risk.
- Enhancing the understanding of DILI mechanisms.
Professional Societies/National and International Groups
The American Association for the Advancement of Science
Member
2010 – 2015
American Chemical Society
Member
2011 – 2015
Society of Toxicology
Member
2013 – Present
Selected Publications
Recent Advances in Understanding the Hepatotoxicity Associated with Protein Kinase Inhibitors.
Shi Q., Yang X., Ren L., and Mattes W.B.
Expert Opin Drug Metab Toxicol. 2020, 16(3):217-226.
Cytotoxicity of 34 FDA Approved Small-Molecule Kinase Inhibitors in Primary Rat and Human Hepatocytes.
Zhang J., Ren L., Yang X., White M., Greenhaw J., Harris T., Wu Q., Bryant M., Papoian T., Mattes W., and Shi Q.
Toxicol Lett. 2018, 291:138-148.
Drug-Induced Liver Injury in Children: Clinical Observations, Animal Models, and Regulatory Status.
Shi Q., Yang X., Greenhaw J.J., Salminen A.T., Russotti G.M., and Salminen WF.
Int J Toxicol. 2017, 36(5):365-379.
Effects of 31 FDA Approved Small-Molecule Kinase Inhibitors on Isolated Rat Liver Mitochondria.
Zhang J., Salminen A., Yang X., Luo Y., Wu Q., White M., Greenhaw J., Ren L., Bryant M., Salminen W., Papoian T., Mattes W., and Shi Q.
Arch Toxicol. 2017, 91(8):2921-2938.
Human Induced Pluripotent Stem Cell-Derived Hepatocyte-Like Cells as a Potential New Tool to Understand Small Molecule Kinase Inhibitors Induced Hepatotoxicity.
Shi Q. and Mattes W.
American Pharmaceutical Review. 2017, 20: 64-67.
The Cytochrome P450 Inhibitor SKF-525A Disrupts Autophagy in Primary Rat Hepatocytes.
Luo Y., Yang X., and Shi Q.
Chem Biol Interact. 2016, 255:55-62.
Circulating MicroRNA and Long Noncoding RNA as Biomarkers of Cardiovascular Diseases.
Shi Q. and Yang X.
J Cell Physiol. 2016, 231(4):751-5.
A Comprehensive Study of the Association Between Drug Hepatotoxicity and Daily Dose, Liver Metabolism, and Lipophilicity using 975 Oral Medications.
Weng Z., Wang K., Li H., and Shi Q.
Oncotarget. 2015, 6(19):17031-8.
Regorafenib Impairs Mitochondrial Functions, Activates AMP-Activated Protein Kinase, Induces Autophagy, and Causes Rat Hepatocyte Necrosis.
Weng Z., Luo Y., Yang X., Greenhaw J.J., Li H., Xie L., Mattes W.B., and Shi Q.
Toxicology. 2015, 327:10-21.
Drugs and Diseases Interacting with Cigarette Smoking in US Prescription Drug Labelling.
Li H. and Shi Q.
Clin Pharmacokinet. 2015, 54(5):493-501.
Circulating Mitochondrial Biomarkers for Drug-Induced Liver Injury.
Shi Q., Yang X., Mattes W.B., Mendrick D.L., Harrill A.H., and Beger R.D.
Biomark Med. 2015, 9(11):1215-23.
Inhibition of Cytochrome P450s Enhances (+)-Usnic Acid Cytotoxicity in Primary Cultured Rat Hepatocytes.
Shi Q., Greenhaw J., and Salminen W.F.
J Appl Toxicol. 2014, 34(8):835-40.
Circulating Extracellular Vesicles as a Potential Source of New Biomarkers of Drug-Induced Liver Injury.
Yang X., Weng Z., Mendrick D.L., and Shi Q.
Toxicol Lett. 2014, 225(3):401-6.
Green Tea Epigallocatechin Gallate Binds to and Inhibits Respiratory Complexes in Swelling but not Normal Rat Hepatic Mitochondria.
Weng Z., Zhou P., Salminen W.F., Yang X., Harrill A.H., Cao Z., Mattes W.B., Mendrick D.L., and Shi Q.
Biochem Biophys Res Commun. 2014, 443(3):1097-104.
Hopes and Challenges in Using miRNAs as Translational Biomarkers for Drug-Induced Liver Injury.
Shi Q., Yang X., and Mendrick D.L.
Biomark Med. 2013, 7(2):307-15.
Mechanisms for Epigallocatechin Gallate Induced Inhibition of Drug Metabolizing Enzymes in Rat Liver Microsomes.
Weng Z., Greenhaw J., Salminen W.F., and Shi Q.
Toxicol Lett. 2012, 214(3):328-38.
Hepatic Cytochrome P450s Attenuate the Cytotoxicity Induced by Leflunomide and its Active Metabolite A77 1726 in Primary Cultured Rat Hepatocytes.
Shi Q., Yang X., Greenhaw J., and Salminen W.F.
Toxicol Sci. 2011, 122(2):579-86.
Biomarkers for Drug-Induced Liver Injury.
Shi Q., Hong H., Senior J., and Tong W.
Expert Rev Gastroenterol Hepatol. 2010, 4(2):225-34.
Gene Expression Profiling in the Developing Rat Brain Exposed to Ketamine.
Shi Q., Guo L., Patterson T.A., Dial S., Li Q., Sadovova N., Zhang X., Hanig J.P., Paule M.G., Slikker W. Jr., and Wang C.
Neuroscience. 2010, 166(3):852-63.
Lab Members
Contact Information for all lab members:
(870) 543-7121
NCTRResearch@fda.hhs.gov
Dustyn Barnette
ORISE Fellow
- Contact Information
- Qiang Shi
- (870) 543-7121
- Expertise
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ExpertiseApproachDomainTechnology & DisciplineToxicology