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Abstract #69029 Published in IGR 18-1
Pro-fibrotic pathway activation in trabecular meshwork and lamina cribrosa is the main driving force of glaucoma
Zhavoronkov A; Kanherkar RR; Izumchenko E; Teka M; Cantor C; Manaye K; Sidransky D; West MD; Makarev E; Csoka ABCell cycle (Georgetown, Tex.) 2016; 15: 1643-1652
See also comment(s) by Tina Wong •
While primary open-angle glaucoma (POAG) is a leading cause of blindness worldwide, it still does not have a clear mechanism that can explain all clinical cases of the disease. Elevated IOP is associated with increased accumulation of extracellular matrix (ECM) proteins in the trabecular meshwork (TM) that prevents normal outflow of aqueous humor (AH) and has damaging effects on the fine mesh-like lamina cribrosa (LC) through which the optic nerve fibers pass. Applying a pathway analysis algorithm, we discovered that an elevated level of TGFβ observed in glaucoma-affected tissues could lead to pro-fibrotic pathway activation in TM and in LC. In turn, activated pro-fibrotic pathways lead to ECM remodeling in TM and LC, making TM less efficient in AH drainage and making LC more susceptible to damage from elevated IOP via ECM transformation in LC. We propose pathway targets for potential therapeutic interventions to delay or avoid fibrosis initiation in TM and LC tissues.
Full article
Classification:
2.5.1 Trabecular meshwork (Part of: 2 Anatomical structures in glaucoma > 2.5 Meshwork)
2.3 Sclera (Part of: 2 Anatomical structures in glaucoma)
2.14 Optic disc (Part of: 2 Anatomical structures in glaucoma)
3.6 Cellular biology (Part of: 3 Laboratory methods)
