ReviewInternational journal of ophthalmology2023
Mitochondrial dysfunction in glaucomatous degeneration.
Review in International journal of ophthalmology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.
- Identifying potential key metabolic pathways and biomarkers in glaucoma: a systematic review and meta-analysis.BMJ open ophthalmology · 2025Pooled it
- AMPK Therapy-A Little Goes A Long Way.Cells · 2026Review
- Diagnostic Role of Multimodal Imaging in Optic Disc Diseases.Diagnostics (Basel, Switzerland) · 2026Review
- Involvement of Mitophagy in Endothelin-1 Mediated Neurodegeneration in Rodent Models of Glaucoma.bioRxiv : the preprint server for biology · 2026Article
- Crosstalk between endoplasmic reticulum stress and mitochondrial homeostasis: A new perspective on ophthalmic disease treatment.Journal of cell communication and signaling · 2026Review
- Extracellular vesicles as therapeutic agents for retinal ganglion cell degeneration: current challenges and future prospects.International ophthalmology · 2026Review
- Deficient autophagy in retinal ganglion cells impairs the degradation of intracellular organelles, leading to neurodegeneration.Cell death & disease · 2026Article
- A paradoxical relationship between mitochondrial calcium regulation and retinal ganglion cell degeneration after axon damage.bioRxiv : the preprint server for biology · 2026Article
- Mitochondrial Transplantation in the Eye: A Review and Evaluation of Surgical Approaches.bioRxiv : the preprint server for biology · 2026Article
- The 5-HT1A receptor antagonist WAY-100635 maleate promotes retinal ganglion cell differentiation and protects the retino-visual circuits.Communications medicine · 2026Article
- Macrophage Migration Inhibitory Factor (MIF)-CD74 Signaling Pathway Mediates Trabecular Meshwork Dysfunction in Glaucoma.bioRxiv : the preprint server for biology · 2026Article
- Mitochondrial ROS in Retinal Neurodegeneration: Thresholds, Quality Control Failure, and Precision Therapeutic Windows.Biomolecules · 2026Review
- Semaglutide Protects Retinal Ganglion Cells Against Rotenone-Induced Degeneration via Improved Glucose Metabolism.Investigative ophthalmology & visual science · 2026Article
- Article
- Circulating eNAMPT in Glaucoma: A Semi-Quantitative Plasma Analysis Before and After Nicotinamide Supplementation.Translational vision science & technology · 2026Article
- Mitochondrial Health Through Nicotinamide Riboside and Berberine: Shared Pathways and Therapeutic Potential.International journal of molecular sciences · 2026Review
- Enzymatic glycosylation as a potential molecular link between Alzheimer's disease and glaucoma.International journal of ophthalmology · 2026Review
- Glucocorticoid-induced RPE injury in ARPE-19 cells: association with excessive autophagy and AMPK/mTOR signaling.International journal of ophthalmology · 2026Article
- Environmental enrichment as a mitochondria-targeting systems strategy across neurodegenerative diseases and retinal dystrophies.Frontiers in neuroscience · 2026Review
- Single-cell profiling of trabecular meshwork identifies mitochondrial dysfunction in a glaucoma model that is protected by vitamin B3 treatment.bioRxiv : the preprint server for biology · 2025Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glaucoma is a kind of optic neuropathy mainly manifested in the permanent death of retinal ganglion cells (RGCs), atrophy of the optic nerve, and loss of visual ability. The main risk factors for glaucoma consist of the pathological elevation of intraocular pressure (IOP) and aging. Although the mechanism of glaucoma remains an open question, a theory related to mitochondrial dysfunction has been emerging in the last decade. Reactive oxygen species (ROS) from the mitochondrial respiratory chain are abnormally produced as a result of mitochondrial dysfunction. Oxidative stress takes place when the cellular antioxidant system fails to remove excessive ROS promptly. Meanwhile, more and more studies show that there are other common features of mitochondrial dysfunction in glaucoma, including damage of mitochondrial DNA (mtDNA), defective mitochondrial quality control, ATP reduction, and other cellular changes, which are worth summarizing and further exploring. The purpose of this review is to explore mitochondrial dysfunction in the mechanism of glaucomatous optic neuropathy. Based on the mechanism, the existing therapeutic options are summarized, including medications, gene therapy, and red-light therapy, which are promising to provide feasible neuroprotective ideas for the treatment of glaucoma.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.