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Glaucoma: Overview

Glaucoma: Overview

Glaucoma is an eye condition characterized by increased intraocular pressure that damages the retina and optic nerve, leading to irreversible blindness if left untreated. The human eye has various components, including the cornea, iris, pupil, lens, and optic nerve. Aqueous humor is secreted by the epithelium of the ciliary body in the posterior chamber and flows through the trabecular meshwork and canal of Schlemm, maintaining normal intraocular pressure. The trabecular meshwork and the canal...

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Related Experiment Video

Updated: Jul 4, 2025

Assessment and Characterization of Hyaloid Vessels in Mice

Assessment and Characterization of Hyaloid Vessels in Mice

Published on: May 15, 2019

Uveitic glaucoma-like features in Yap conditional knockout mice.

Juliette Bitard¹, Elodie-Kim Grellier², Sophie Lourdel²

¹Université Paris-Saclay, CNRS, Institut des Neurosciences Paris-Saclay, Saclay, France. juliette.bitard@universite-paris-saclay.fr.

Cell Death Discovery

|January 25, 2024

Summary

The transcriptional coactivator YAP is crucial for maintaining eye health. Its absence in Müller glia and ciliary body cells leads to glaucoma-like symptoms, including optic nerve damage and vision loss.

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Last Updated: Jul 4, 2025

Assessment and Characterization of Hyaloid Vessels in Mice

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Published on: May 15, 2019

Full-Circle Cauterization of Limbal Vascular Plexus for Surgically Induced Glaucoma in Rodents

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A Laser-induced Mouse Model of Chronic Ocular Hypertension to Characterize Visual Defects

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Published on: August 14, 2013

Area of Science:

Ophthalmology
Neuroscience
Molecular Biology

Background:

Glaucoma is a leading cause of irreversible vision loss, characterized by optic nerve degeneration.
Current treatments for glaucoma are insufficient, necessitating a deeper understanding of early disease mechanisms.
The transcriptional coactivator YAP is recognized for its role in maintaining ocular homeostasis.

Purpose of the Study:

To investigate the role of YAP in ocular integrity and its potential involvement in glaucoma pathogenesis.
To elucidate the consequences of YAP deletion in specific retinal and ciliary body cells.

Main Methods:

Conditional knockout (cKO) mice with Yap deletion in Müller glia and ciliary body non-pigmented epithelial cells were generated.
Phenotypic analysis included assessment of the aqueous-blood barrier, ciliary body structure, and glaucoma-like features.
Transcriptomic analysis was performed on Yap cKO retinas to identify early molecular changes.

Main Results:

Yap cKO mice exhibited aqueous-blood barrier breakdown and ciliary body collapse, mirroring phenotypes in human uveitis samples.
Aged Yap cKO mice displayed glaucoma-like features: Müller-derived protein deregulation, retinal vascular defects, optic nerve degeneration, and retinal ganglion cell death.
Transcriptomic analysis revealed early dysregulation of extracellular matrix genes in Yap cKO retinas.

Conclusions:

YAP plays an essential role in maintaining the structural integrity of the ciliary body and protecting retinal ganglion cells.
YAP deficiency contributes to the development of uveitic glaucoma-like features, highlighting its neuroprotective function.
Targeting YAP pathways may offer novel therapeutic strategies for preventing glaucoma progression.