Journal of Clinical and Experimental Ophthalmology
Open Access
ISSN: 2155-9570
ISSN: 2155-9570
Emmanuel Buys
Scientific Tracks Abstracts: J Clin Exp Ophthalmol
Primary open angle glaucoma (POAG) is a leading cause of blindness worldwide. The molecular signaling involved remains largely unknown. Currently, there is no cure for POAG, available therapies offer incomplete protection, and the disease often goes undetected until irreparable damage has been done. Together, these considerations highlight the need for novel therapeutic approaches, drug targets, and biomarkers. We recently reported that female mice lacking the α1 subunit of the nitric oxide (NO) receptor soluble guanylate cyclase (sGCα1 -/- mice) develop POAG, characterized by age-related RNFL thinning, loss of retinal ganglion cells, and optic neuropathy in the setting of an open iridocorneal angle. The optic neuropathy associated with sGCα1-deficiency was accompanied by modestly increased intraocular pressure and retinal vascular dysfunction. In addition, we identified a variant in the GUCY1A3/ GUCY1B3 locus (encoding the α 1 and β 1 subunit genes of sGC, arranged in tandem) that was associated with POAG. Together, these data provide new insights into the pathogenesis and genetics of POAG and identify sGC as a potential therapeutic target for POAG.
Emmanuel Buys obtained his Ph.D. from the Department of Molecular Biology, Gent University and Flanders Institute of Biotechnology. He is currently an Assistant Professor in Anesthesia at the Massachusetts General Hospital where he studies the role of nitric oxide-cGMP signaling in systemic hypertension (funded by the American heart Association) and primary open angle glaucoma (Funded by an NIH-R01). He has co-authored 46 manuscripts since 2006.