Table of Contents
ISRN Ophthalmology
Volume 2013, Article ID 261386, 14 pages
Review Article

New Therapeutic Targets for Intraocular Pressure Lowering

1Department of Sense Organs, Faculty of Medicine, University of Porto, 4200-319 Porto, Portugal
2Department of Ophthalmology, São João Hospital, 4200-319 Porto, Portugal
3Department of Physiology and Cardiothoracic Surgery, Faculty of Medicine, University of Porto, 4200-319 Porto, Portugal

Received 13 May 2013; Accepted 30 May 2013

Academic Editors: T. Mimura and M. Sugimoto

Copyright © 2013 A. Rocha-Sousa et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Primary open-angle glaucoma (POAG) is a leading cause of irreversible and preventable blindness and ocular hypertension is the strongest known risk factor. With current classes of drugs, management of the disease focuses on lowering intraocular pressure (IOP). Despite of their use to modify the course of the disease, none of the current medications for POAG is able to reduce the IOP by more than 25%–30%. Also, some glaucoma patients show disease progression despite of the therapeutics. This paper examines the new described physiological targets for reducing the IOP. The main cause of elevated IOP in POAG is thought to be an increased outflow resistance via the pressure-dependent trabecular outflow system, so there is a crescent interest in increasing trabecular meshwork outflow by extracellular matrix remodeling and/or by modulation of contractility/TM cytoskeleton disruption. Modulation of new agents that act mainly on trabecular meshwork outflow may be the future hypotensive treatment for glaucoma patients. There are also other agents in which modulation may decrease aqueous humour production or increase uveoscleral outflow by different mechanisms from those drugs available for glaucoma treatment. Recently, a role for the ghrelin-GHSR system in the pathophysiology modulation of the anterior segment, particularly regarding glaucoma, has been proposed.