Targeting Schlemm's Canal in the Medical Therapy of Glaucoma: Current and Future Considerations

Adv Ther. 2017 May;34(5):1049-1069. doi: 10.1007/s12325-017-0513-z. Epub 2017 Mar 27.

Abstract

Schlemm's canal (SC) is a unique, complex vascular structure responsible for maintaining fluid homeostasis within the anterior segment of the eye by draining the excess of aqueous humour. In glaucoma, a heterogeneous group of eye disorders afflicting approximately 60 million individuals worldwide, the normal outflow of aqueous humour into SC is progressively hindered, leading to a gradual increase in outflow resistance, which gradually results in elevated intraocular pressure (IOP). By and large available antiglaucoma therapies do not target the site of the pathology (SC), but rather aim to decrease IOP by other mechanisms, either reducing aqueous production or by diverting aqueous flow through the unconventional outflow system. The present review first outlines our current understanding on the functional anatomy of SC. It then summarizes existing research on SC cell properties; first in the context of their role in glaucoma development/progression and then as a target of novel and emerging antiglaucoma therapies. Evidence from ongoing research efforts to develop effective antiglaucoma therapies targeting SC suggests that this could become a promising site of future therapeutic interventions.

Keywords: Actin polymerization inhibitors; Adenosine receptor agonists; Antiglaucoma drug development; Aqueous humour; Glaucoma; Intraocular pressure; Nitric oxide donors; Ophthalmology; Rho Kinase inhibitors; Schlemm’s canal.

Publication types

  • Review

MeSH terms

  • Aqueous Humor / drug effects*
  • Glaucoma / drug therapy*
  • Humans
  • Intraocular Pressure / drug effects*
  • Nitric Oxide Donors / therapeutic use*
  • Purinergic P1 Receptor Agonists / therapeutic use*
  • Trabecular Meshwork / drug effects*
  • rho-Associated Kinases / antagonists & inhibitors
  • rho-Associated Kinases / therapeutic use*

Substances

  • Nitric Oxide Donors
  • Purinergic P1 Receptor Agonists
  • rho-Associated Kinases