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Trabecular Meshwork Response to Pressure Elevation in the Living Human Eye
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TRPV4 subserves physiological and pathological elevations in intraocular pressure.

Sarah N Redmon1, Monika Lakk1, Yun-Ting Tseng1

  • 1University of Utah.

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|July 23, 2024
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Summary

Ocular hypertension (OHT) involves TRPV4 channels regulating eye pressure. Targeting TRPV4 may offer new glaucoma treatments by improving fluid outflow through the trabecular meshwork.

Keywords:
TRPV4glaucomaintraocular pressureoutflow facilitytrabecular meshwork

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Area of Science:

  • Ophthalmology
  • Physiology
  • Molecular Biology

Background:

  • Ocular hypertension (OHT) increases irreversible vision loss risk.
  • Physiological nightly intraocular pressure (IOP) elevations occur without adverse effects.
  • The pressure sensors regulating physiological vs. pathological OHT and their impact on trabecular meshwork (TM) outflow are unknown.

Purpose of the Study:

  • To identify pressure sensors regulating OHT.
  • To investigate the role of these sensors in TM outflow regulation.
  • To explore potential therapeutic targets for glaucoma.

Main Methods:

  • Investigated TRPV4 (a stretch-activated cation channel) in OHT models in mice.
  • Administered TRPV4 agonists and antagonists.
  • Utilized conventional outflow-specific Trpv4 knockdown.
  • Assessed outflow facility in 3D nanoscaffolds.

Main Results:

  • TRPV4 activation is required for OHT induced by circadian rhythm, iridocorneal angle occlusion, and glucocorticoids.
  • TRPV4 antagonists lowered IOP in nocturnal OHT, steroid-induced hypertension, and microbead-induced hypertension models.
  • Trpv4 knockdown lowered IOP and protected retinal neurons.
  • TRPV4 inhibition enhanced outflow facility in TM-populated nanoscaffolds.

Conclusions:

  • Tonic TRPV4 signaling in the TM drives outflow resistance.
  • TRPV4 is a critical mechanosensor in the conventional outflow pathway.
  • TRPV4 represents a potential novel therapeutic target for managing OHT and glaucoma.