Current understanding of conventional outflow dysfunction in glaucoma.

Published

Journal Article (Review)

Regulation of intraocular pressure by the conventional (trabecular) outflow pathway is complicated, involving a myriad of mechanical and chemical signals. In most, intraocular pressure is maintained within a tight range over a lifetime. Unfortunately in some, dysfunction results in ocular hypertension and open-angle glaucoma. In the context of established knowledge, this review summarizes recent investigations of conventional outflow function, with the goal of identifying areas for future inquiry and therapeutic targeting.Mechanical stimulation of conventional outflow cells due to intraocular pressure fluctuations impacts contractility, gene expression, pore formation, enzyme activity, and signaling. Numerous local signaling mediators in the conventional pathway such as bioactive lipids, cytokines, nitric oxide, and nucleotides participate in the regulation of outflow. Interestingly outflow through the conventional pathway is not uniform, but segmental, with passageways constantly changing due to focal protease activity of trabecular cells clearing extracellular matrix materials. The relationship between extracellular matrix expression and trabecular meshwork contractility appears to coordinately impact outflow resistance and is the target of a new class of drugs, the Rho kinase inhibitors.The conventional outflow pathway is a dynamic, pressure-sensitive tissue that is vulnerable to pathology on many fronts, each representing a therapeutic opportunity.

Full Text

Duke Authors

Cited Authors

  • Stamer, WD; Acott, TS

Published Date

  • March 2012

Published In

Volume / Issue

  • 23 / 2

Start / End Page

  • 135 - 143

PubMed ID

  • 22262082

Pubmed Central ID

  • 22262082

Electronic International Standard Serial Number (EISSN)

  • 1531-7021

International Standard Serial Number (ISSN)

  • 1040-8738

Digital Object Identifier (DOI)

  • 10.1097/ICU.0b013e32834ff23e

Language

  • eng