New Insights Into Pathophysiological Mechanisms Regulating Conventional Aqueous Humor Outflow

Abstract

The aim of the article was to overview the pathophysiology of the conventional outflow pathway, trabecular meshwork, and intraocular pressure and to discuss the options of future glaucoma treatment directed to improvement in aqueous outflow. The literature search in the Medline, Embase, and Cochrane databases from April to May 2012 was performed; a total of 47 articles analyzed. The diminished conventional pathway may be altered by several pathophysiological mechanisms like TM obstruction caused by transforming growth factor-β2, clastic nondeformable cells, macrophages leaking from hypermature cataract, iris pigment, lens capsular fragments after YAG-laser posterior capsulotomy, proteins and their subfragments. It is known that trabecular meshwork contraction reduces outflow, and the actomyosin system is directly linked to this mechanism. New glaucoma drugs are still under investigation, but it is already proven that agents such as latranculin-B are effective in improving aqueous drainage. Selective Rho-associated coiled coilforming protein kinase inhibitors have been shown to cause a significant improvement in outflow facility and may become a new option for glaucoma treatment. Caldesmon negatively regulates actin-myosin interactions and thus increases outflow. Stem cells may replace missing or nonfunctional trabecular meshwork cells and hopefully will bring a new treatment solution. Pathophysiological mechanisms regulating conventional aqueous humor outflow are still not fully understood and require further investigations. Future treatment decisions should be directed to a specific mechanism regulating an elevation in intraocular pressure.

The synergistic effect of inflammation and metabolic syndrome on intraocular pressure

“…An alteration in the ECM may cause an increased resistance in the trabecular meshwork and a consequent decrease in outflow. [24,25] Our results support the idea that systemic inflammation may result in an increase in intraocular pressure. In line with our finding, Cellini et al [22] previously reported a significant association between systemic endothelial dysfunction and open-angle glaucoma.…”

Gender-Specific Association Between Serum Uric Acid and Incident High Intraocular Pressure in Chinese Population: A Cross-Sectional Study

“… 30 Mucopolysaccharides of endothelial cells were related to macrophage function and were involved in the components of the ECM. 12 The change in the ECM might lead to an increase in the resistance of the trabecular meshwork, resulting in a decrease in outflow, 31 , 32 which might induce high IOP. Our results supported the view that systemic inflammation might lead to increased IOP.…”

Evaluation of Outflow StructuresIn Vivoafter the Phacocanaloplasty

“…The conventional drainage route of aqueous humor occurs via the trabecular meshwork (TM), Schlemm's canal (SC), collector channels, and aqueous veins and then streams into episcleral venous circulation. Appropriate secretion and regulation of aqueous humor are essential for normal eye function [ 2 ].…”