Absence of trabecular meshwork-inducible stretch response ( TISR )/oculomedin gene and proximal promoter mutation in primary open angle glaucoma patients

2000 ◽  
Vol 107 (4) ◽  
pp. 404-405 ◽  
Author(s):  
Y.F. Leung ◽  
L. Baum ◽  
D.S.C. Lam ◽  
D.S.P. Fan ◽  
J.K.H. Chua ◽  
...  
Keyword(s):  
Trabecular Meshwork ◽  
Primary Open Angle Glaucoma ◽  
Open Angle Glaucoma ◽  
Proximal Promoter ◽  
Open Angle ◽  
Promoter Mutation ◽  
Stretch Response

scholarly journals Neuroinflammation in Primary Open-Angle Glaucoma

2020 ◽  
Vol 9 (10) ◽  
pp. 3172 ◽  
Author(s):  
Stefania Vernazza ◽  
Sara Tirendi ◽  
Anna Maria Bassi ◽  
Carlo Enrico Traverso ◽  
Sergio Claudio Saccà
Keyword(s):  
Oxidative Stress ◽  
Immune Response ◽  
Trabecular Meshwork ◽  
Primary Open Angle Glaucoma ◽  
Open Angle Glaucoma ◽  
Glaucoma Surgery ◽  
Open Angle ◽  
Antioxidant Defences ◽  
Age Related ◽  
Wide Range

Primary open-angle glaucoma (POAG) is the second leading cause of irreversible blindness worldwide. Increasing evidence suggests oxidative damage and immune response defects are key factors contributing to glaucoma onset. Indeed, both the failure of the trabecular meshwork tissue in the conventional outflow pathway and the neuroinflammation process, which drives the neurodegeneration, seem to be linked to the age-related over-production of free radicals (i.e., mitochondrial dysfunction) and to oxidative stress-linked immunostimulatory signaling. Several previous studies have described a wide range of oxidative stress-related makers which are found in glaucomatous patients, including low levels of antioxidant defences, dysfunction/activation of glial cells, the activation of the NF-κB pathway and the up-regulation of pro-inflammatory cytokines, and so on. However, the intraocular pressure is still currently the only risk factor modifiable by medication or glaucoma surgery. This present review aims to summarize the multiple cellular processes, which promote different risk factors in glaucoma including aging, oxidative stress, trabecular meshwork defects, glial activation response, neurodegenerative insults, and the altered regulation of immune response.

scholarly journals Role of Fibronectin in Primary Open Angle Glaucoma

Cells ◽  
2019 ◽  
Vol 8 (12) ◽  
pp. 1518 ◽  
Author(s):  
Jennifer A. Faralli ◽  
Mark S. Filla ◽  
Donna M. Peters
Keyword(s):  
United States ◽  
Trabecular Meshwork ◽  
Vision Loss ◽  
Primary Open Angle Glaucoma ◽  
Open Angle Glaucoma ◽  
The United States ◽  
Open Angle ◽  
Cell Matrix ◽  
Fibronectin Fibrils

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.

scholarly journals Detection of Differentially Expressed Glycogenes in Trabecular Meshwork of Eyes with Primary Open-Angle Glaucoma

2006 ◽  
Vol 47 (4) ◽  
pp. 1491 ◽  
Author(s):  
Shiri Diskin ◽  
Janardan Kumar ◽  
Zhiyi Cao ◽  
Joel S. Schuman ◽  
Tim Gilmartin ◽  
...  
Keyword(s):  
Trabecular Meshwork ◽  
Primary Open Angle Glaucoma ◽  
Open Angle Glaucoma ◽  
Differentially Expressed ◽  
Open Angle
Sign in / Sign up

Export Citation Format

Share Document