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Open Angle Glaucoma: Treatment

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In open-angle glaucoma, the iridocorneal angle remains open, but the trabecular meshwork becomes stiff, slowing down the outflow of aqueous humor. This causes a buildup of aqueous humor in the anterior chamber, leading to a sudden increase in intraocular pressure. The treatment for open-angle glaucoma focuses on reducing the elevated intraocular pressure by either decreasing the secretion of aqueous humor or increasing its outflow.
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Related Experiment Video

Updated: Jun 26, 2026

Laser Capture Microdissection of Highly Pure Trabecular Meshwork from Mouse Eyes for Gene Expression Analysis

Laser Capture Microdissection of Highly Pure Trabecular Meshwork from Mouse Eyes for Gene Expression Analysis

Published on: June 3, 2018

[TGF-beta2 involvements in open angle glaucoma].

C Stefan¹, L Dragomir, Diana Melinte Dumitrică

¹Clinica de Oftalmologie, Spitalul Clinic de Urgenţă Militar Central.

Oftalmologia (Bucharest, Romania : 1990)

|January 20, 2009

Summary

Transforming growth factor beta2 (TGF beta2) is elevated in primary open angle glaucoma (POAG) patients. This cytokine may contribute to POAG by altering the trabecular meshwork extracellular matrix.

Related Experiment Videos

Last Updated: Jun 26, 2026

Laser Capture Microdissection of Highly Pure Trabecular Meshwork from Mouse Eyes for Gene Expression Analysis

Laser Capture Microdissection of Highly Pure Trabecular Meshwork from Mouse Eyes for Gene Expression Analysis

Published on: June 3, 2018

Area of Science:

Ophthalmology
Molecular Biology
Biochemistry

Context:

Primary open angle glaucoma (POAG) is a leading cause of irreversible blindness worldwide.
The pathogenesis of POAG involves complex molecular mechanisms affecting the trabecular meshwork.
Identifying key molecular players is crucial for understanding POAG progression.

Purpose:

To investigate the correlation between transforming growth factor beta2 (TGF beta2) levels and POAG.
To quantify TGF beta2 concentration in the aqueous humor of POAG patients and control subjects.

Summary:

An observational study compared TGF beta2 levels in aqueous humor between 17 POAG patients and 16 healthy controls using ELISA.
Results showed significantly higher TGF beta2 concentrations in patients with POAG compared to the control group.
This suggests TGF beta2 plays a role in the altered extracellular matrix turnover characteristic of POAG.

Impact:

The findings highlight TGF beta2 as a potential biomarker and therapeutic target in POAG.
Understanding TGF beta2's profibrotic effect on the trabecular meshwork could lead to novel treatment strategies.
This research contributes to the molecular understanding of glaucoma pathophysiology.