Future target molecules in antiglaucoma therapy: tgf-Beta may have a role to play

Ophthalmic Res. 2010;43(1):1-10. doi: 10.1159/000246571. Epub 2009 Oct 14.

Abstract

Glaucoma, a leading cause of irreversible blindness, is often associated with increased resistance to aqueous outflow in trabecular tissue. Increased outflow resistance has been attributed to increased extracellular matrix (ECM) deposition in trabecular tissue. A critical balance between the synthesis and breakdown of the components of extracellular tissue is important in keeping the intraocular pressure within the normal range. Multiple mechanisms have been shown to affect ECM turnover in trabecular tissue. In this review, we examine the related literature to understand the role of TGF-beta in ECM turnover, in the development and progression of glaucoma, and in possible therapeutic strategies that can be devised by targeting the TGF-beta signaling pathways.

Publication types

  • Review

MeSH terms

  • Animals
  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology
  • Anti-Inflammatory Agents, Non-Steroidal / therapeutic use
  • Antihypertensive Agents / pharmacology
  • Antihypertensive Agents / therapeutic use
  • Disease Progression
  • Extracellular Matrix / drug effects
  • Extracellular Matrix / metabolism
  • Glaucoma / drug therapy*
  • Glaucoma / etiology
  • Glaucoma / metabolism
  • Humans
  • Intraocular Pressure / drug effects
  • Signal Transduction / drug effects
  • Trabecular Meshwork / drug effects
  • Trabecular Meshwork / metabolism
  • Trabecular Meshwork / physiopathology
  • Transforming Growth Factor beta* / antagonists & inhibitors
  • Transforming Growth Factor beta* / physiology

Substances

  • Anti-Inflammatory Agents, Non-Steroidal
  • Antihypertensive Agents
  • Transforming Growth Factor beta