Staff Fellow — Division of Systems Biology
Li Pang, M.D., M.S.
Dr. Pang received an M.D. from North China Coal Medical College, China in 1993 with the second highest grade point average among 300+ students. As a result, she was selected to enter the most prestigious hospital in China (Peking Union Medical College Hospital) for further training in endocrinology and started her research career in the cardiovascular field. In 1998, Dr. Pang received a scholarship from the University of Montreal and later joined the Montreal Heart Institute to study ion channel remolding in heart failure and atrial fibrillation. In 2005, she was recruited as a faculty member of the Department of Pharmacology & Toxicology at the University of Arkansas for Medical Sciences (UAMS), where she collaborated with other scientists and developed an NIH-funded RO1 project to provide novel long-term therapy for hypertension. She was one of the principle investigators (PI) of a two-PI grant. In December 2011, Dr. Pang joined FDA as a commissioner’s fellow and received intensive regulatory science training. Upon graduation, she was converted to an FDA staff fellow and joined NCTR officially in December 2013. Currently, Dr. Pang is serving as the PI on three NCTR protocols, one of which is supported by the FDA Center for Drug Evaluation and Research (CDER). Dr. Pang has established wide and diverse collaborations with scientist from other FDA centers,, academia, and industry and she received the NCTR Director's Award in 2015 and 2018. She also received a CDER Director's Special Citation Award in 2018.
Dr. Pang’s research interests have included ion channel remodeling in cardiovascular disease, pharmacogenetics, gene therapy, and biomarker identification. Her current research goals are to use a wide range of techniques including cellular and molecular biology, biochemistry, viral gene transduction, patch clamp, microelectrode array, impedance, and high-resolution imaging to comprehensively characterize human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) for detection of drug-induced cardiotoxicity. She is also interested in using the hiPSC-CMs model to investigate genetic and hormonal effects in sex differences of drug-induced QT prolongation and Torsade de Pointes. A third ongoing project uses human iPSC-CMs for prediction of personalized kinase inhibitor-induced cardiotoxicity.
Professional Societies/National and International Groups
American Association for Cancer Research
2012 – 2015
Health and Environmental Sciences Institute (HESI) Cardiac Safety Committee
2014 – Present
HESI Cardiac Stem Cell Working Group
2014 – Present
Society of Toxicology
2015 – Present
Safety Pharmacology Society
2016 – Present
International Multisite Study of Human-Induced Pluripotent Stem Cell-Derived Cardiomyocytes for Drug Proarrhythmic Potential Assessment.
Blinova K., Dang Q., Millard D., Smith G., Pierson J., Guo L., Brock M., Lu H.R., Kraushaar U., Zeng H., Shi H., Zhang X., Sawada K., Osada T., Kanda Y., Sekino Y., Pang L., Feaster T.K., Kettenhofen R., Stockbridge N., Strauss D.G., and Gintant G.
Cell Rep. 2018, 24(13):3582-3592. doi: 10.1016/j.celrep.2018.08.079.
Sex-Related Differences in Drug-Induced QT Prolongation and Torsades de Pointes: A New Model System with Human iPSC-CMs.
Huo J., Wei F., Cai C., Lyn-Cook B., and Pang L.
Toxicol Sci. 2018, doi: 10.1093/toxsci/kfy239. [Epub ahead of print]
Evaluation of Batch Variations in Induced Pluripotent Stem Cell-Derived Human Cardiomyocytes from 2 Major Suppliers.
Huo J., Karmalakar A., Yang X., Word B., Stockbridge N., Lyn-Cook B., and Pang L.
Toxicol Sci. 2017,156(1):25-38. doi: 10.1093/toxsci/kfw235.
Comprehensive Translational Assessment of Human Induced Pluripotent Stem Cell Derived Cardiomyocytes for Evaluating Drug-Induced Arrhythmias.
Blinova K., Stohlman J., Vicente J., Chan D., Johannesen L., Hortigon-Vinagre M., Zamora V., Smith G., Crumb W., Pang L., Lyn-Cook B., Ross J., Brock M., Chvatal S., Millard D., Galeotti L., Stockbridge N., and Strauss D.
Toxicol Sci. 2016, pii: kfw200. [Epub ahead of print]
MicroRNA-Mediated Maturation of Human Pluripotent Stem Cell-Derived Cardiomyocytes: Towards a Better Model for Cardiotoxicity?
White M., Pang L., and Yang X.
Food Chem Toxicol. 2016, pii: S0278-6915(16)30180-6. doi: 10.1016/j.fct.2016.05.025. [Epub ahead of print]
Reversal of MicroRNA Dysregulation in an Animal Model of Pulmonary Hypertension.
Gubrij I., Pangle A., Pang L., and Johnson L.
PLoS One. 2016, 11(1):e0147827. doi: 10.1371/journal.pone.0147827. eCollection 2016.
ATP-Binding Cassette Genes Genotype and Expression: A Potential Association with Pancreatic Cancer Development and Chemoresistance?
Pang L., Word B., Xu J., Wang H., Hammons G., Huang S., and Lyn-Cook B.
Gastroenterol Res Pract. 2014, 2014:414931. doi: 10.1155/2014/414931. Epub 2014 May 5.
Angiotensin II Upregulates Ca(V)1.2 Protein Expression in Cultured Arteries via Endothelial H(2)O(2) Production.
Wang W., Pang L., and Palade P.
J Vasc Res. 2011, 48(1):67-78. doi: 10.1159/000318776. Epub 2010 Jul 14.
High-Conductance, Ca(2+) -Activated K+ Channels: Altered Expression Profiles in Aging and Cardiovascular Disease.
Pang L. and Rusch N.
Mol Interv. 2009, 9(5):230-3. doi: 10.1124/mi.9.5.6.
Vascular Smooth Muscle-Specific Knockdown of the Noncardiac Form of the L-type Calcium Channel by MicroRNA-Based Short Hairpin RNA as a Potential Antihypertensive Therapy.
Rhee S., Stimers J., Wang W., and Pang L.
J Pharmacol Exp Ther. 2009, 329(2):775-82. doi: 10.1124/jpet.108.148866. Epub 2009 Feb 24.
Angiotensin II Causes Endothelial-Dependent Increase in Expression of Ca(V)1.2 Protein in Cultured Arteries.
Wang W., Pang L., and Palade P.
Eur J Pharmacol. 2008, 599(1-3):117-20. doi: 10.1016/j.ejphar.2008.09.034. Epub 2008 Sep 30.
Characterization of the Cardiac KCNE1 Gene Promoter.
Mustapha Z., Pang L., and Nattel S.
Cardiovasc Res. 2007, 73(1):82-91. Epub 2006 Nov 10.
Vascular-Specific Increase in Exon 1B-Encoded CAV1.2 Channels in Spontaneously Hypertensive Rats.
Wang W., Saada N., Dai B., Pang L., and Palade P.
Am J Hypertens. 2006, 19(8):823-31.
Tissue-Specific Expression of Two Human Ca(v)1.2 Isoforms Under the Control of Distinct 5' Flanking Regulatory Elements.
Pang L., Koren G., Wang Z., and Nattel S.
FEBS Lett. 2003, 546(2-3):349-54.
Effects of Angiotensin-Converting Enzyme Inhibition on the Development of the Atrial Fibrillation Substrate in Dogs with Ventricular Tachypacing-Induced Congestive Heart Failure.
Li D., Shinagawa K., Pang L., Leung T., Cardin S., Wang Z., and Nattel S.
Circulation. 2001, 104(21):2608-14.
Characterization of a Putative Insulin-Responsive Element and Its Binding Protein(s) in Rat Angiotensinogen Gene Promoter: Regulation by Glucose and Insulin.
Chen X., Zhang S., Pang L., Filep J., Tang S., Ingelfinger J., and Chan J.
Endocrinology. 2001, 142(6):2577-85.
Molecular Mechanism(s) of Insulin Action on the Expression of the Angiotensinogen Gene in Kidney Proximal Tubular Cells.
Wu X., Chen X., Zhang S., Pang L., To C., Wang T., Hohman T., Filep J., and Chan J.
J Renin Angiotensin Aldosterone Syst. 2000, 1(2):166-74.
The Study of Mutation in Exon 17 of Insulin Receptor Gene in Essential Hypertensive Pedigrees.
[Article in Chinese]
Pang L., Sun M., Guo D., Guan B., and Ji B.
Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 1997, 19(2):83-8.
Contact information for all lab members:
Chengzhong Cai, M.D., Ph.D.
Feng Wei, M.D., Ph.D.
Lijun Ren, M.D.
- Contact Information
- Li Pang
- (870) 543-7121
ExpertiseApproachDomainTechnology & DisciplineToxicology