About My Research
Dr. Hoang's main research interest is in molecular signaling that regulates vascular abnormality in diabetic retinopathy with the goal of identifying a molecular target, which can correct vascular defects. His current research project focuses on answering a mysterious question: why are humans highly susceptible to diabetic retinopathy while rodents are not? By answering this question, he hopes to develop a rodent diabetic retinopathy model for testing drugs and for unraveling molecular mechanism that protects retinal vascular dysfunction.
Education
1994: BSc, Biochemistry, First Class Honor, University of London, Royal Holloway College, England, UK
1998: PhD, Biochemistry and Molecular Biology, University of Leeds, England, UK
Postgraduate Training
2000: Fellowship, Welcome Trust Center for Cell Matrix Research, University of Manchester, England, UK
2010: Fellowship, Beth Israel Deaconess Medical Center and Harvard Medical School Center for Vascular Biology Research
Academic Appointments
2010-present: Instructor in Ophthalmology, Harvard Medical School
Professional Memberships
2010-present: Mass. Eye and Ear Alumni Association
2004-present: American Society for Cell Biology
1998-present: UK Biochemical Society
Honors
1991-1994: Driver Prize, University of London, Royal Holloway College
1994-1998: British Medical Research Council (MRC) Instant Award Studentship
- Receptor interacting protein kinase 3 (RIP3) regulates iPSCs generation through modulating cell cycle progression genes. Stem Cell Res. 2019 03; 35:101387.
- Issues with the Specificity of Immunological Reagents for NLRP3: Implications for Age-related Macular Degeneration. Sci Rep. 2018 01 11; 8(1):461.
- Anti-inflammatory activity of Barleria lupulina: Identification of active compounds that activate the Nrf2 cell defense pathway, organize cortical actin, reduce stress fibers, and improve cell junctions in microvascular endothelial cells. J Ethnopharmacol. 2016 Dec 04; 193:397-407.
- Effects of metformin on retinoblastoma growth in vitro and in vivo. Int J Oncol. 2014 Dec; 45(6):2311-24.
- Active Rac1 improves pathologic VEGF neovessel architecture and reduces vascular leak: mechanistic similarities with angiopoietin-1. Blood. 2011 Feb 03; 117(5):1751-60.
- Moderation of calpain activity promotes neovascular integration and lumen formation during VEGF-induced pathological angiogenesis. PLoS One. 2010 Oct 25; 5(10):e13612.
- Cdc42-mediated inhibition of GSK-3ß improves angio-architecture and lumen formation during VEGF-driven pathological angiogenesis. Microvasc Res. 2011 Jan; 81(1):34-43.
- Calpain inhibitors reduce retinal hypoxia in ischemic retinopathy by improving neovascular architecture and functional perfusion. Biochim Biophys Acta. 2011 Apr; 1812(4):549-57.
- Moderate GSK-3ß inhibition improves neovascular architecture, reduces vascular leakage, and reduces retinal hypoxia in a model of ischemic retinopathy. Angiogenesis. 2010 Sep; 13(3):269-77.
- Down syndrome candidate region 1 isoform 1 mediates angiogenesis through the calcineurin-NFAT pathway. Mol Cancer Res. 2006 Nov; 4(11):811-20.
- In vivo and in vitro models of Mammalian angiogenesis. Methods Mol Biol. 2005; 294:269-85.
- Rho activity critically and selectively regulates endothelial cell organization during angiogenesis. Proc Natl Acad Sci U S A. 2004 Feb 17; 101(7):1874-9.
Show More
Show Less