Abstract
Primary open angle glaucoma (POAG) is the most common form of glaucoma and the 2nd most common cause of irreversible vision loss in the United States. Nearly 67 million people have the disease worldwide including >3 million in the United States. A major risk factor for POAG is an elevation in intraocular pressure (IOP). The increase in IOP is believed to be caused by an increase in the deposition of extracellular matrix proteins, in particular fibronectin, in a region of the eye known as the trabecular meshwork (TM). How fibronectin contributes to the increase in IOP is not well understood. The increased density of fibronectin fibrils is thought to increase IOP by altering the compliance of the trabecular meshwork. Recent studies, however, also suggest that the composition and organization of fibronectin fibrils would affect IOP by changing the cell-matrix signaling events that control the functional properties of the cells in the trabecular meshwork. In this article, we will discuss how changes in the properties of fibronectin and fibronectin fibrils could contribute to the regulation of IOP.
Highlights
Introduction to GlaucomaGlaucoma is an age-related, heterogeneous group of neurodegenerative diseases that results in damage to the optic nerve and irreversible blindness
InJCT, the normal eye, especially fibronectin, which is believed to contribute to the increase in resistance to aqueous humor outflow resistance in this region would be lowered through relaxation of the contractile fibroblastic-like outflow through the trabecular meshwork (TM)/s canal (SC)
In Primary open angle glaucoma (POAG), there is a buildup of extracellular matrix (ECM) proteins within the juxtacanalicular tissue (JCT), especially fibronectin, which is believed to contribute to the increase in resistance to aqueous humor outflow through the TM/SC
Summary
Glaucoma is an age-related, heterogeneous group of neurodegenerative diseases that results in damage to the optic nerve and irreversible blindness. InJCT, the normal eye, especially fibronectin, which is believed to contribute to the increase in resistance to aqueous humor outflow resistance in this region would be lowered through relaxation of the contractile fibroblastic-like outflow through the TM/SC Such alterations in the expression of ECM proteins are thought to lead to changes in theadjacent biological characteristics of resident cells the JCT, which more andciliary more acquire cells in the JCT and the sclera. In POAG, there is a buildup of extracellular matrix (ECM) proteins within the JCT, especially fibronectin, which is believed to contribute to the increase in resistance to aqueous humor outflow through the TM/SC Such alterations in the expression of ECM proteins are thought to lead to changes in the biological characteristics of resident cells in the JCT, which more and more acquire the structural and functional characteristics of contractile myofibroblasts [6,7,8]. These changes to the contractility of the actomyosin network are likely to be transmitted by the surrounding ECM via integrins
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
