Purchase this article with an account.
Ted S Acott; Trabecular Meshwork EMC in Glaucoma. Invest. Ophthalmol. Vis. Sci. 201657(12):.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
Presentation Description :
Elevated intraocular pressure (IOP) is the primary risk factor and currently the only treatable parameter for glaucoma. IOP is normally regulated by modulation of the aqueous humor outflow resistance, which is thought to resides within the deepest portion of the trabecular meshwork and the inner wall endothelium of Schlemm's canal (SC). Most of the resistance is found within a zone of extracellular matrix (ECM) within approximately 10 μm of the inner wall SC cell's basal surface. This outflow resistance ECM is produced and turned over in a highly regulated manner by the TM and SC cells in this juxtacanalicular region. Evidence supporting models of an additional direct contribution of SC cells to the outflow resistance, involving SC pore formation, has also recently appeared. This outflow resistance, comprised primarily of ECM with some apparent SC cell pore involvement, is continually being remodeled and adjusted by these TM and SC cells in response to sustained fluctuations in the IOP. These fluctuation appear to sense by these cells as mechanical stretching and distortion. Thus, a common hallmark of glaucomatous IOP elevation is the loss of this IOP homeostatic capability, where IOP fluctuations trigger compensatory outflow resistance adjustments, and consequently result in disregulation of the outflow resistance.
This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.
This PDF is available to Subscribers Only