| First Author | Buys ES | Year | 2013 |
| Journal | PLoS One | Volume | 8 |
| Issue | 3 | Pages | e60156 |
| PubMed ID | 23527308 | Mgi Jnum | J:199535 |
| Mgi Id | MGI:5502994 | Doi | 10.1371/journal.pone.0060156 |
| Citation | Buys ES, et al. (2013) Soluble guanylate cyclase alpha1-deficient mice: a novel murine model for primary open angle glaucoma. PLoS One 8(3):e60156 |
| abstractText | Primary open angle glaucoma (POAG) is a leading cause of blindness worldwide. The molecular signaling involved in the pathogenesis of POAG remains unknown. Here, we report that mice lacking the alpha1 subunit of the nitric oxide receptor soluble guanylate cyclase represent a novel and translatable animal model of POAG, characterized by thinning of the retinal nerve fiber layer and loss of optic nerve axons in the context of an open iridocorneal angle. The optic neuropathy associated with soluble guanylate cyclase alpha1-deficiency was accompanied by modestly increased intraocular pressure and retinal vascular dysfunction. Moreover, data from a candidate gene association study suggests that a variant in the locus containing the genes encoding for the alpha1 and beta1 subunits of soluble guanylate cyclase is associated with POAG in patients presenting with initial paracentral vision loss, a disease subtype thought to be associated with vascular dysregulation. These findings provide new insights into the pathogenesis and genetics of POAG and suggest new therapeutic strategies for POAG. |
