Abstract
Primary Open-Angle Glaucoma (POAG), an optic neuropathy that is a leading cause of irreversible blindness, has been studied extensively in hopes of better understanding its underlying mechanism. Glucocorticoids (GC) are commonly used to treat inflammatory ocular conditions but are also known to increase the risk of glaucoma by raising Intraocular Pressure (IOP) in susceptible individuals, leading to steroid- induced glaucoma. Based on clinical studies as well as molecular experiments, steroid-induced glaucoma and POAG show many similarities, including a common underlying mechanism of IOP elevation. Studying steroid-induced glaucoma can reveal more about the pathways underlying decreased outflow of aqueous humor and POAG. GCs have been shown to cause numerous structural changes in the Trabecular Meshwork (TM), including thickening of trabecular beams, activation of TM cells and increased deposition of extracellular material. GCs also upregulate the expression of MYOC (myocilin) in human TM, a gene whose mutation is linked to 10% of juvenile glaucoma cases. Other studies demonstrate that GCs downregulate PLAT, which codes for tissue Plasminogen Activator (tPA) and decrease Matrix Metalloproteinase (MMP) gene expression. In addition, tPA administration has been shown to prevent GC-induced IOP elevation in sheep eyes. The present review demonstrates some of the important interactions between GCs and the TM that can lead to novel therapeutic measures in the setting of steroid- induced glaucoma as well as POAG.
Highlights
Primary Open-Angle Glaucoma (POAG) is an optic neuropathy that currently stands as one of the leading causes of irreversible, yet preventable, blindness in the world (Quigley, 1996)
Factors that regulate aqueous humor outflow and Extracellular Matrix (ECM) remodeling are of great interest to researchers, as this information would allow for better control of intraocular pressure (IOP) and novel treatments of ocular hypertension, steroid-induced glaucoma and POAG
GC effects on gene expression, including MYOC, PLAT and Matrix Metalloproteinase (MMP) has opened up new avenues of exploration for pathways that are involved in regulation of aqueous outflow
Summary
Primary Open-Angle Glaucoma (POAG) is an optic neuropathy that currently stands as one of the leading causes of irreversible, yet preventable, blindness in the world (Quigley, 1996). Factors that regulate aqueous humor outflow and ECM remodeling are of great interest to researchers, as this information would allow for better control of IOP and novel treatments of ocular hypertension, steroid-induced glaucoma and POAG. The exact mechanism of steroid-induced IOP elevation is unknown, it is thought to result from increased aqueous humor outflow resistance at the trabecular meshwork through various biochemical and morphological changes (Rohen et al, 1973).
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