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Related Concept Videos

Open Angle Glaucoma: Treatment01:27

Open Angle Glaucoma: Treatment

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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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Angle Closure Glaucoma: Treatment01:28

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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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Glaucoma: Overview01:25

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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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Related Experiment Video

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CD38-NAD(+) Axis: New Insights into Glaucoma Therapy.

Wenyige Zhang1,2,3, Haina Zheng1,2, Yulian Pang1,2,4

  • 1Jiangxi Provincial Key Laboratory for Ophthalmology, Nanchang University School of Ophthalmology & Optometry, Nanchang, 330006, Jiangxi, China.

Molecular Neurobiology
|July 22, 2025
PubMed
Summary

Nicotinamide adenine dinucleotide (NAD+) depletion and CD38 enzyme activity are key in glaucoma progression, driving retinal ganglion cell (RGC) damage. Targeting the CD38/NAD+ axis may offer new neuroprotective therapies for glaucoma.

Keywords:
CD38GlaucomaNAD +NeuroprotectionTherapeutic strategies

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Area of Science:

  • Ophthalmology
  • Neuroscience
  • Biochemistry

Background:

  • Glaucoma is a leading cause of irreversible blindness associated with retinal ganglion cell (RGC) degeneration.
  • Mitochondrial dysfunction and NAD+ depletion are implicated in glaucoma pathogenesis.
  • CD38, an enzyme regulating NAD+, is increasingly recognized for its role in glaucoma.

Purpose of the Study:

  • To review the interplay between NAD+ and CD38 in glaucoma.
  • To explore therapeutic strategies targeting the CD38/NAD+ axis for glaucoma treatment.

Main Methods:

  • Systematic review of existing literature on NAD+, CD38, and glaucoma.
  • Analysis of studies investigating CD38 inhibition and NAD+ precursor supplementation in glaucoma models.

Main Results:

  • CD38 activity increases with age, reducing NAD+ levels and contributing to RGC injury.
  • Inhibiting CD38 or supplementing with NAD+ precursors can protect RGCs and mitigate glaucoma-related damage.
  • CD38 modulates oxidative stress, inflammation, and apoptosis in glaucoma.

Conclusions:

  • The CD38/NAD+ axis presents a promising therapeutic target for glaucoma.
  • Further research is needed to address challenges like drug selectivity and efficacy validation for clinical application.