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Related Concept Videos

Open Angle Glaucoma: Treatment01:27

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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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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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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...
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Whole Vitreous Humor Dissection for Vitreodynamic Analysis
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Deconstructing aqueous humor outflow - The last 50 years.

Paul L Kaufman1

  • 1University of Wisconsin - Madison, School of Medicine & Public Health, Dept of Ophthalmology & Visual Sciences, United States.

Experimental Eye Research
|June 27, 2020
PubMed
Summary

Research explores primate aqueous humor outflow, revealing ciliary muscle and trabecular meshwork roles. Novel therapies like gene and stem cell treatments show promise for enhancing outflow and reducing intraocular pressure.

Keywords:
Actin cytoskeletonAqueous humor outflowGene therapyGlaucomaIntraocular pressureMechanosensitivityNitric oxideStem cell therapy

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Area of Science:

  • Ophthalmology
  • Primate Research
  • Molecular Biology

Background:

  • Aqueous humor outflow is crucial for regulating intraocular pressure (IOP).
  • The ciliary muscle (CM) and trabecular meshwork (TM) are key structures involved in aqueous humor drainage.
  • Understanding outflow mechanisms is vital for developing effective glaucoma treatments.

Purpose of the Study:

  • To review and summarize decades of research on primate aqueous humor outflow.
  • To investigate the effects of various pharmacological agents and cellular manipulations on outflow facility.
  • To explore the potential of novel therapeutic strategies, including gene and stem cell therapies, for glaucoma.

Main Methods:

  • Experiments involved primate eyes, including iris removal, ciliary muscle disinsertion, and treatment with various drugs (cytochalasins, latrunculins, epinephrine, phalloidin, H-7, ML7, Y27632, nitric oxide donors, adenosine A1 agonists, angiotensin II, prostaglandin F2α analogues).
  • Optical coherence tomography (OCT) and optical imaging were used to visualize outflow pathways.
  • Gene therapy vectors were introduced via intracameral or sub-tenon injections in live non-human primates (NHP) and monkey organ cultured anterior segments (MOCAS).
  • Human organ cultured anterior segments (HOCAS) were used to study trabecular meshwork cell function.

Main Results:

  • Disinserting the ciliary muscle abolished pilocarpine's effect on outflow facility, while epinephrine increased facility in these eyes.
  • Cytochalasins and latrunculins increased outflow facility; combinations with epinephrine showed synergistic effects.
  • Prostaglandin F2α analogues increased matrix metalloproteinase synthesis, remodeling the extracellular matrix and increasing uveoscleral outflow.
  • Gene therapy showed promise in lab models, with reporter genes persisting in NHP TM for over two years.
  • Intracameral injection of a PGF synthase vector reduced IOP in NHP, but the effect was less potent and shorter-lived than topical PGF2α analogues.

Conclusions:

  • The ciliary muscle and trabecular meshwork play critical roles in regulating aqueous humor outflow and IOP.
  • Pharmacological agents targeting cytoskeletal dynamics and signaling pathways can modulate outflow facility.
  • Gene and stem cell therapies hold significant potential for treating glaucoma by enhancing aqueous outflow, though challenges remain in achieving sustained efficacy and overcoming 'turn-off' mechanisms.
  • Further research into targeted delivery methods, like intracanalicular injection, and understanding regulatory pathways is needed to optimize these novel therapies.