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Related Concept Videos

Open Angle Glaucoma: Treatment01:27

Open Angle Glaucoma: Treatment

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...
Angle Closure Glaucoma: Treatment01:28

Angle Closure Glaucoma: Treatment

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...
Glaucoma: Overview01:25

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: Jun 16, 2026

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

Targeting Rap1-YAP1 mechanosignaling for ameliorating acute IOP elevation-induced trabecular meshwork dysfunction.

Yupeng Zhang1, Xue Li2, Qiumei Hu2

  • 1School of Life Sciences, Tsinghua University, Beijing 100084, China.

Iscience
|June 15, 2026
PubMed
Summary
This summary is machine-generated.

Glaucoma

Keywords:
Molecular biologyOphthalmology

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Trabecular Meshwork Response to Pressure Elevation in the Living Human Eye
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A Magnetic Microbead Occlusion Model to Induce Ocular Hypertension-Dependent Glaucoma in Mice
09:26

A Magnetic Microbead Occlusion Model to Induce Ocular Hypertension-Dependent Glaucoma in Mice

Published on: March 23, 2016

Area of Science:

  • Ophthalmology
  • Cell Biology
  • Mechanobiology

Background:

  • Glaucoma is a leading cause of blindness, with elevated intraocular pressure (IOP) as a key modifiable risk factor.
  • The trabecular meshwork (TM) is crucial for IOP regulation and is mechanosensitive, but its response to high IOP is not fully understood.

Purpose of the Study:

  • To investigate human trabecular meshwork (TM) cell responses to mechanical stimuli and acute ocular hypertension.
  • To explore the role of Rap1-YAP1 mechanosignaling in TM cell damage and fibrotic changes.

Main Methods:

  • Single-cell sequencing of human TM cells.
  • Establishment of in vivo and in vitro models of acute ocular hypertension.
  • Analysis of TM cell death, cytoskeletal rearrangement, fibrotic biomarker expression, and YAP1/Rap1 signaling.

Main Results:

  • Acute IOP elevation induced TM cell death, cytoskeletal rearrangement, and fibrotic biomarker upregulation in human and mouse models.
  • Phosphorylated YAP1 and Rap1 levels were reduced following acute IOP elevation.
  • Rap1b knockin mice showed protection against TM damage and YAP1 upregulation after acute IOP elevation.

Conclusions:

  • Human TM cells are susceptible to mechanical stress from elevated IOP.
  • The Rap1-YAP1 mechanosignaling pathway is implicated in TM cell response to acute IOP elevation.
  • Targeting Rap1-YAP1 mechanosignaling may offer a novel therapeutic strategy for protecting the TM in glaucoma.