Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Open Angle Glaucoma: Treatment01:27

Open Angle Glaucoma: Treatment

583
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.
Drugs such as carbonic anhydrase inhibitors, α2- and...
583
Angle Closure Glaucoma: Treatment01:28

Angle Closure Glaucoma: Treatment

702
Angle-closure glaucoma, or closed-angle glaucoma, is an eye condition where the iris bulges out and blocks the iridocorneal angle, resulting in a buildup of aqueous humor and increased intraocular pressure. Immediate medical attention is necessary due to the sudden onset of symptoms. The treatment for angle-closure glaucoma includes short-term and long-term approaches. Short-term treatment involves using eye drops like pilocarpine to lower intraocular pressure by increasing aqueous humor...
702
Glaucoma: Overview01:25

Glaucoma: Overview

777
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...
777

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

A novel interpretable deep learning-based computational framework designed synthetic enhancers with broad cross-species activity.

Nucleic acids research·2024
Same author

Normative Profile of Retinal Nerve Fiber Layer Thickness and Lamina Cribrosa-Related Parameters in a Healthy Non-Glaucoma Cynomolgus Monkey Colony.

Translational vision science & technology·2024
Same author

Retrocorneal membrane interception enhanced penetrating canaloplasty for patients with open angle glaucoma secondary to ICE syndrome.

International ophthalmology·2024
Same author

Impact of Acute Short-Term Hypobaric Hypoxia on Anterior Chamber Geometry.

Journal of glaucoma·2024
Same author

Associations of static and dynamic iris parameters in healthy Chinese individuals: the Handan Eye Study.

Eye (London, England)·2024
Same author

The S341P mutant MYOC renders the trabecular meshwork sensitive to cyclic mechanical stretch.

Heliyon·2024

Related Experiment Video

Updated: Sep 16, 2025

Laser Capture Microdissection of Highly Pure Trabecular Meshwork from Mouse Eyes for Gene Expression Analysis
13:47

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

Published on: June 3, 2018

9.4K

Trabecular meshwork: A pivotal target for evolving glaucoma treatments.

Yue Wan1, Xinzheng Guo2, Ningli Wang3

  • 1Department of Ophthalmology, Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing Institute of Ophthalmology, Beijing Key Laboratory of Ophthalmology & Visual Sciences, Beijing 100730, China.

Survey of Ophthalmology
|July 10, 2025
PubMed
Summary

The trabecular meshwork (TM) regulates intraocular pressure (IOP). TM dysfunction contributes to glaucoma, but new therapies targeting TM offer hope for improved IOP control and glaucoma management.

Keywords:
Cell therapyGene therapyGlaucomaIntraocular pressureLaser trabeculoplastyMinimally invasive glaucoma surgeryNitric oxide donorsRho kinase inhibitorsTrabecular meshwork

More Related Videos

Trabecular Meshwork Response to Pressure Elevation in the Living Human Eye
09:03

Trabecular Meshwork Response to Pressure Elevation in the Living Human Eye

Published on: June 20, 2015

10.1K
Full-Circle Cauterization of Limbal Vascular Plexus for Surgically Induced Glaucoma in Rodents
10:10

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

Published on: February 15, 2022

1.5K

Related Experiment Videos

Last Updated: Sep 16, 2025

Laser Capture Microdissection of Highly Pure Trabecular Meshwork from Mouse Eyes for Gene Expression Analysis
13:47

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

Published on: June 3, 2018

9.4K
Trabecular Meshwork Response to Pressure Elevation in the Living Human Eye
09:03

Trabecular Meshwork Response to Pressure Elevation in the Living Human Eye

Published on: June 20, 2015

10.1K
Full-Circle Cauterization of Limbal Vascular Plexus for Surgically Induced Glaucoma in Rodents
10:10

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

Published on: February 15, 2022

1.5K

Area of Science:

  • Ophthalmology
  • Cell Biology
  • Biomedical Engineering

Background:

  • The trabecular meshwork (TM) is crucial for regulating intraocular pressure (IOP) by controlling aqueous humor outflow.
  • Pathological changes in the TM, including reduced cellularity and increased stiffness, elevate IOP and contribute to glaucoma.
  • Understanding TM structure, cellularity, biomechanics, and molecular dysfunction is key to glaucoma pathogenesis.

Purpose of the Study:

  • To review the anatomical, cellular, and biomechanical properties of the TM.
  • To outline TM alterations in various glaucoma subtypes and identify molecular mechanisms of TM dysfunction.
  • To discuss current and emerging therapies targeting the TM for glaucoma management.

Main Methods:

  • Literature review of TM anatomy, physiology, and pathology.
  • Analysis of molecular pathways implicated in TM dysfunction (e.g., Rho GTPase, NO, TGF-β2).
  • Overview of therapeutic strategies, including pharmacologic, non-invasive, surgical, gene, and cell-based approaches.

Main Results:

  • TM dysfunction is central to glaucoma pathogenesis, involving altered cellularity, matrix turnover, and biomechanical properties.
  • Key molecular pathways like Rho GTPase signaling, NO pathways, TGF-β2-induced fibrosis, lipid signaling, and ER stress contribute to TM dysfunction.
  • A range of TM-targeted therapies are advancing, showing promise for IOP control.

Conclusions:

  • Targeting the trabecular meshwork offers a promising avenue for glaucoma treatment and IOP management.
  • Emerging gene and cell-based therapies represent novel regenerative strategies for restoring TM function.
  • Continued innovation in delivery methods, efficacy, and safety is essential for optimizing TM-targeted interventions in glaucoma care.