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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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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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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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Related Experiment Video

Updated: Mar 29, 2026

Doppler Optical Coherence Tomography of Retinal Circulation
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Peripheral Blood Mononuclear Cell Oxygen Consumption and Systemic Bioenergetics in Glaucoma Management.

Chun Hsiung1,2, Ta-Hung Chiu3, Wei-Ting Yen1,2

  • 1Department of Ophthalmology, Tri-Service General Hospital, Taipei 114202, Taiwan.

International Journal of Molecular Sciences
|March 28, 2026
PubMed
Summary

Glaucoma progression may be driven by metabolic issues, not just eye pressure. Systemic metabolic profiling offers new ways to assess risk and develop neuroprotective treatments targeting mitochondrial function.

Keywords:
glaucomamitochondrial dysfunctionneurodegenerationneuroprotectionoxidative stressoxygen consumptionperipheral blood mononuclear cellretinal ganglion cells

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Area of Science:

  • Ophthalmology
  • Neuroscience
  • Mitochondrial Biology

Background:

  • Glaucoma involves progressive retinal ganglion cell loss, often continuing despite lowered intraocular pressure (IOP).
  • IOP-independent mechanisms, including metabolic failure and mitochondrial dysfunction, are critical drivers of glaucoma.
  • A shift from a pressure-centric to a bioenergetic model is needed to understand glaucoma pathogenesis.

Purpose of the Study:

  • To review the shift towards a bioenergetic model in glaucoma research.
  • To analyze the role of mitochondrial function and systemic metabolic biomarkers in glaucoma.
  • To explore novel therapeutic targets for glaucoma based on metabolic dysfunction.

Main Methods:

  • Review of studies on mitochondrial function in glaucoma patients.
  • Analysis of peripheral blood mononuclear cell (PBMC) oxygen consumption rates.
  • Assessment of systemic nicotinamide adenine dinucleotide (NAD+) levels and Complex I activity.
  • Examination of SARM1-mediated axonal degeneration and mitophagy markers.

Main Results:

  • Glaucoma patients show reduced PBMC oxygen consumption and lower systemic NAD+ levels.
  • Compromised systemic respiratory function correlates with faster visual field loss and structural thinning, irrespective of IOP.
  • Evidence points to Complex I defects, SARM1 activation, and impaired mitophagy in glaucoma.

Conclusions:

  • Systemic metabolic profiling is a valuable tool for glaucoma risk assessment.
  • Targeting mitochondrial bioenergetics (e.g., with nicotinamide, pyruvate, CoQ10, metformin) shows therapeutic potential.
  • Understanding glaucoma's bioenergetic basis opens new avenues for neuroprotection.