In This Section

Hong Wang, MD, PhD, EMBA

Laura H. Carnell Professor
Director and Professor, Center for Metabolic Disease Research
Professor, Cardiovascular Research Center
Professor, Sol Sherry Thrombosis Research Center
Professor, Microbiology, Immunology and Inflammation

Hong Wang
Contact Information

Contact Information



About Me

Research Interests

The Wang laboratory studies pathological and metabolic changes in cardiovascular diseases, including hyperlipidemia, hyperglycemia, hyperinsulinemia, hyperhomocysteinemia, obesity, vascular inflammation, diabetes, stroke, peripheral artery disease, myocardial infarction, and chronic kidney disease. Researches focus on investigating the effect and underlying mechanism of metabolic disorder on 1) Atherosclerosis and vascular inflammation, 2) Endothelial function, 3), Monocyte epitope mapping/polarization, 4) HDL metabolism, 5) Epigenetic modification, and 6) Gene and stem cell therapy. We use dynamic state-of-art technologies to dissect disease mechanism and identify potential therapeutic targets. Frequently used research approaches include metabolomics, transcriptomics, RNA-Seq, CHIP-Seq, chemical, biochemical, immunological and pathophysiological approaches, microsurgery models for various vascular disease and thrombosis, transgenic and gene knock-out mice.

Education, Training & Credentials

Educational Background

  • EMBA, The Fox School of Business, Temple University, Philadelphia, PA, 2009
  • Postdoctoral Fellow, Harvard School of Public Health, Boston, 1997
  • PhD, University of Montreal,  Montreal, Canada 1996
  • MSc, Peking Union Medical College, Beijing, China,1985
  • MD, Jiang Xi Medical School, Nanchang, China, 1979

Digital Bibliography

11806997. Wang H, Yoshizumi M, Lai K-H, Tsai J-C, Haber E, Lee M-E Inhibition of growth and p21ras methylation in vascular endothelial cells by homocysteine but not cysteine. J Biol Chem (1997) 272:25380-25385

11806997. Wang H‡, Jiang XH, Yang F, Chapman GB, Durante W, Sibinga NES, Schafer AI, Cyclin A transcriptional suppression is the major mechanism mediating homocysteine-induced endothelial cell growth inhibition, Blood, (2002) 99:939-945, ‡ Corresponding author,

12506016. Wang H‡, Jiang XH, Yang F, Gaubatz JW, Ma L, Magera MJ, Yang XF, Berger PB, Durante W, Pownall HJ, Schafer AI, Hyperhomocysteinemia accelerates atherosclerosis in cystathionine -synthase and apolipoprotein E double knockout mice with and without dietary perturbation, Blood, (2004) 101:3901-3907, ‡ Corresponding author... Expand