ReviewFrontiers in neuroscience2017
Metabolic Vulnerability in the Neurodegenerative Disease Glaucoma.
Review in Frontiers in neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
58 citing papers in PubMed, 91 citations in OpenAlex.
- Involvement of Mitophagy in Endothelin-1 Mediated Neurodegeneration in Rodent Models of Glaucoma.bioRxiv : the preprint server for biology · 2026Article
- Pharmacological restoration of impaired autophagy in retinal ganglion cells prevents abnormal mitochondrial accumulation and glaucomatous neurodegeneration.Molecular neurodegeneration · 2026Article
- Intraocular pressure induced blood retinal barrier compromise in mouse models and human glaucoma.Nature communications · 2026Article
- The 5-HT1A receptor antagonist WAY-100635 maleate promotes retinal ganglion cell differentiation and protects the retino-visual circuits.Communications medicine · 2026Article
- Cell-intrinsic vulnerability and immune activation cooperate to drive degeneration in a mitochondrial complex I deficiency model of optic neuropathy.Journal of neuroinflammation · 2026Article
- Targeting the Glutaminolysis Pathway in Glaucoma-Associated Fibrosis.International journal of molecular sciences · 2025Review
- Review
- "Optic nerve of steel": A case of very high intraocular pressures with markedly little visual field progression over years.American journal of ophthalmology case reports · 2025Article
- Pyruvate and related energetic metabolites modulate resilience against high genetic risk for glaucoma.eLife · 2025Article
- Pyruvate and Related Energetic Metabolites Modulate Resilience Against High Genetic Risk for Glaucoma.bioRxiv : the preprint server for biology · 2025Article
- Loss of Sarm1 Mitigates Axonal Degeneration and Promotes Neuronal Repair After Ischemic Stroke.bioRxiv : the preprint server for biology · 2025Article
- Article
- Glaucoma, Pseudoexfoliation and Hearing Loss: A Systematic Literature Review.Journal of clinical medicine · 2024Review
- The ketogenic diet and hypoxia promote mitophagy in the context of glaucoma.Frontiers in cellular neuroscience · 2024Article
- Efficacy of a Spearmint (Mentha spicata L.) Extract as Nutritional Support in a Rat Model of Hypertensive Glaucoma.Translational vision science & technology · 2023Article
- Oxidative Stress Induced Dysfunction of Protein Synthesis in 661W Mice Photoreceptor Cells.Proteomes · 2023Article
- Aging Effects on Optic Nerve Neurodegeneration.International journal of molecular sciences · 2023Review
- Activation of autophagy inhibits the activation of NLRP3 inflammasome and alleviates sevoflurane-induced cognitive dysfunction in elderly rats.BMC neuroscience · 2023Article
- Astrocytes of the eye and optic nerve: heterogeneous populations with unique functions mediate axonal resilience and vulnerability to glaucoma.Frontiers in ophthalmology · 2023Article
- Role of mitophagy in ocular neurodegeneration.Frontiers in neuroscience · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Axons can be several orders of magnitude longer than neural somas, presenting logistical difficulties in cargo trafficking and structural maintenance. Keeping the axon compartment well supplied with energy also presents a considerable challenge; even seemingly subtle modifications of metabolism can result in functional deficits and degeneration. Axons require a great deal of energy, up to 70% of all energy used by a neuron, just to maintain the resting membrane potential. Axonal energy, in the form of ATP, is generated primarily through oxidative phosphorylation in the mitochondria. In addition, glial cells contribute metabolic intermediates to axons at moments of high activity or according to need. Recent evidence suggests energy disruption is an early contributor to pathology in a wide variety of neurodegenerative disorders characterized by axonopathy. However, the degree to which the energy disruption is intrinsic to the axon vs. associated glia is not clear. This paper will review the role of energy availability and utilization in axon degeneration in glaucoma, a chronic axonopathy of the retinal projection.
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What OpenQuestion holds
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.