For glaucoma, elevated pressure in the eye is the most common risk factor, an optic neuropathy that can cause blindness and affects more than 67 million people worldwide.
Elevated eye pressure in glaucoma develops due to abnormal functioning of the trabecular meshwork (TM) causing intraocular fluid to back up. Next-generation glaucoma drugs will target the finely tuned mechanisms of the TM that maintain normal intraocular pressure, as described in an article in Journal of Ocular Pharmacology and Therapeutics, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers. The article, one of 25 articles in a special double issue of the Journal, is available free on the Journal of Ocular Pharmacology and Therapeutics website.
The article "Intraocular Pressure Homeostasis: Maintaining Balance in a High-Pressure Environment," by Ted Acott and coauthors, Oregon Health & Science University, Portland, OR, describes the efficient mechanisms at work in the eye to keep intraocular pressure within an acceptable range for 92-98% of the population. Understanding these mechanisms will enable the development of drug interventions to treat the unfortunate 2-8% of people that are at risk of developing elevated eye pressure and glaucoma.
The special double issue provides a comprehensive look at the TM and next-generation glaucoma therapies in development through a collection of editorials, original research articles, and reviews. Included is the review article "The Role of TGF-ß2 and Bone Morphogenetic Proteins in the Trabecular Meshwork and Glaucoma," in which Robert Wordinger, Tasneem Sharma, and Abbot Clark, University of North Texas Health Science Center, Fort Worth, describe the TGF-ß superfamily of growth factors and their role in primary open-angle glaucoma (POAG), the second leading cause of blindness worldwide.
Also of note, Nelson Winkler, Mayo Clinic College of Medicine, and Michael Fautsch, Mayo Clinic, Rochester, MN, explore the current understanding of how prostaglandin analogues, first-line treatments for glaucoma, work to reduce elevated intraocular pressure, in the review article "Effects of Prostaglandin Analogues on Aqueous Humor Outflow Pathways."