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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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NAD+ supplementation improves mitochondrial functions and normalizes glaucomatous trabecular meshwork features.

Yameng Liu1, Qianwen Bu1, Die Hu2

  • 1State Key Laboratory Cultivation Base, Shandong Provincial Key Laboratory of Ophthalmology, Shandong Eye Institute, Shandong First Medical University & Shandong Academy of Medical Sciences, Qingdao, 266071, China.

Experimental Cell Research
|June 19, 2024
PubMed
Summary

Glaucoma involves high intraocular pressure (IOP) damaging the trabecular meshwork (TM). Restoring mitochondrial function with NAD+ supplementation may offer a new glaucoma treatment by improving TM cell health.

Keywords:
GlaucomaMitochondriaNAD(+) precursorsTrabecular meshwork

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Area of Science:

  • Ophthalmology
  • Cell Biology
  • Mitochondrial Medicine

Background:

  • Glaucoma is a leading cause of irreversible vision loss, characterized by elevated intraocular pressure (IOP).
  • Dysfunctional trabecular meshwork (TM) cells contribute to elevated IOP, and current treatments lack efficacy.
  • Mitochondrial function is critical for maintaining TM cell health and regulating IOP.

Purpose of the Study:

  • To investigate the role of mitochondrial dysfunction in glaucomatous TM cells.
  • To explore the potential of NAD+ supplementation as a therapeutic strategy for glaucoma.

Main Methods:

  • Primary TM cells were treated with dexamethasone to mimic glaucomatous changes.
  • Glaucomatous TM cell line (GTM3) and normal TM cell line (iHTM) were compared for mitochondrial function.
  • NAD+ levels, mitochondrial membrane potential, phagocytic function, and oxidative respiration were assessed.
  • The expression of NAD+-consuming enzymes CD38 and PARP1 was analyzed.

Main Results:

  • Glaucomatous TM cells exhibited cytoskeletal abnormalities, increased extracellular matrix, and disrupted mitochondrial dynamics.
  • GTM3 cells showed impaired mitochondrial membrane potential, reduced phagocytic capacity, and decreased oxidative respiration compared to iHTM cells.
  • Lower NAD+ levels were observed in GTM3 cells, correlated with increased CD38 and PARP1 expression.
  • NAD+ supplementation restored mitochondrial function and cellular viability in GTM3 cells.

Conclusions:

  • Aberrant mitochondrial function in glaucomatous TM cells is linked to increased NAD+ consumption via CD38 and PARP1.
  • NAD+ supplementation shows promise in ameliorating mitochondrial dysfunction and improving TM cell function.
  • NAD+ supplementation represents a potential novel therapeutic approach for glaucoma treatment.