Hong Wang, MD, PhD, EMBA

Hong Wang

Hong Wang, MD, PhD, EMBA

  • Lewis Katz School of Medicine

      • Laura H. Carnell Professor

    • Center for Metabolic Disease Research

      • Director and Professor

    • Cardiovascular Research Center

      • Professor

    • Sol Sherry Thrombosis Research Center

      • Professor

    • Microbiology, Immunology and Inflammation

      • Professor

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

  • 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

Publications

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
16226235. Tan HM, Jiang XH, Yang F, Li ZH, Liao D, Trial J, Magera M, Durante W, Yang XF, Wang H, Hyperhomocysteinemia inhibits post injury re-endothelialization in mice, Cardiovascular Res, (2006) 69:253-262

16226235. Jiang XH, Yang F, Tan HM, Liao D, Bryan RM Jr., Durante W, Rumbaut RE, Yang XF, Wang H, Hyperhomocysteinemia impairs endothelial function and eNOS activity via protein kinase C activation, Arterioscler Thromb Vasc Biol., (2005) 25:2515-2521

16931800. Liao D, Tan HM, Hui RT, Li ZH, Jiang XH, Yang F, Gaubatz JW, Durante W, Chan L, Schafer AI, Pownall HJ, Yang XF, Wang H. Hyperhomocysteinemia Decreases Circulating High-Density Lipoprotein by Inhibiting Apolipoprotein A-I Protein Synthesis and Enhancing HDL Cholesterol Clearance. Circ. Res. (2006) 99:598-606, [Accompanied by an Editorial: Circ. Res. 99:565-566]

17715404. Jiang XH, Yang F, Brailoiu E, Jakubowski H, Dun NJ, Schafer AI, Yang XF, Durante W and Wang H, Differential regulation of homocysteine transport in vascular endothelial and smooth muscle cells, Arterioscler. Thromb. Vasc. Biol. (2007) 27:1976-83

17698632. Jamaluddin SM, Chen I, Yang F, Jiang XH, Jan M, Liu XM, Schafer AI, Durante W, Yang XF, and Wang H, Homocysteine inhibits endothelial cell growth via DNA hypomethylation of the cyclin A gene. Blood (2007) 110:3648-3655, [Accompanied by an Editorial: Blood,110:3495-3496]

19578482. Yang, XF, Yin, Y, Wang, H, Vascular inflammation and atherosclerosis are activated via receptors for PAMPs and suppressed by regulatory T cells. Drug Discovery Today, (2008)5:125-142

19858416. Zhang, D, Jiang, X, Pu, F, Yan Y, Song, J, Gupta, S, Schafer, AI, Durante, W, Kruger, W, Yang, XF and Wang, H., Hyperhomocysteinemia promotes inflammatory monocyte generation and accelerates atherosclerosis in transgenic CBS deficient mice. Circulation (2009) 120:1893-1902

20305127. Chen NC, Yang F, Capecci LM, Gu ZY, Schafer AI, Durante W, Yang XF, Wang H, Regulation of homocysteine metabolism and methylation in human and mouse tissues, The FASEB Journal, (2010) 24(8):2804-17

21653942. Cheng ZJ, Jiang XH, Kruger WD, Praticò D, Gupta S, Mallilankaran K, Muniswamy M, Schafer AI, Durante W, Yang XF, Wang H, Hyperhomocysteinemia impairs endothelium-derived hyperpolarizing factor-mediated vasorelaxation in transgenic cystathionine beta-synthase-deficient mice, Blood, (2011) 118:1998-2006 [Accompanied by an Editorial: Blood,118:1717-1719

22202099. Pansuria M, Xi H, Li L, Yang XF, Wang H. (2012) Insulin resistance, metabolic stress, and atherosclerosis, Frontiers in Bioscienc 1;4:916-31

22628578. Zhang DQ, Fang P, Jiang XH, Nelson J, Moore JK, Kruger WD, Berretta RM, Houser SR, Yang XF, Wang H, Severe hyperhomocysteinemia promotes bone marrow-derived and resident inflammatory monocyte differentiation and atherosclerosis in LDLr/CBS-deficient mice, (2012) Circ Res, 111:37-49