ReviewNeural regeneration research2023
Regulatory mechanisms of retinal ganglion cell death in normal tension glaucoma and potential therapies.
Review in Neural regeneration research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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Who cites it
23 citing papers in PubMed, 32 citations in OpenAlex.
- Neurotoxic effects of dietary glutamate in glaucoma and potential nutritional and pharmacological therapies: a scoping review.International ophthalmology · 2026Article
- Analysis of Pediatric Secondary Glaucoma Patients Treated with Micropulse Transscleral Cyclophotocoagulation (MP-TSCPC).Life (Basel, Switzerland) · 2026Article
- Research Advances in Glanimal Models of Glaucoma: Exploring Multidimensional Mechanisms and Novel Therapeutic Strategies.Pharmaceutics · 2026Review
- Gap junction protein connexin 36 proteostatic mechanisms in photoreceptor cells subjected to excitotoxic stress.Acta biochimica Polonica · 2026Article
- CD40-CD154 Interactions Induced Progressive Neurodegeneration in Acute Ocular Hypertension Mice.Investigative ophthalmology & visual science · 2025Article
- Integrating neuroprotection, antioxidative effects, and precision medicine in glaucoma management with bioactive compounds.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025Review
- AAV2-driven endothelin induces chronic reduced retinal blood flow/retinal ganglion cell loss in rats.Life science alliance · 2025Article
- Retinal Vessel Diameter Reductions Are Associated with Retinal Ganglion Cell Dysfunction, Thinning of the Ganglion Cell and Inner Plexiform Layers, and Decreased Visual Field Global Indices in Glaucoma Suspects.Diagnostics (Basel, Switzerland) · 2025Article
- The relationship between aldosterone-induced retinal ganglion cell loss, blood pressure, and intraocular pressure.Japanese journal of ophthalmology · 2025Article
- Ferroptosis Contributes to Retinal Ganglion Cell Loss in GLAST Knockout Mouse Model of Normal Tension Glaucoma.Investigative ophthalmology & visual science · 2025Article
- Comparative Proteomic Study of Retinal Ganglion Cells Undergoing Various Types of Cellular Stressors.bioRxiv : the preprint server for biology · 2024Article
- Exploring the Ocular Surface Microbiome and Tear Proteome in Glaucoma.International journal of molecular sciences · 2024Article
- Apoptosis in glaucoma: A new direction for the treatment of glaucoma (Review).Molecular medicine reports · 2024Review
- A time window for rescuing dying retinal ganglion cells.Cell communication and signaling : CCS · 2024Article
- Unlocking the potential for optic nerve regeneration over long distances: a multi-therapeutic intervention.Frontiers in neurology · 2024Review
- Transcriptomic analysis of plasma-derived small extracellular vesicles reveals the pathological characteristics of normal tension glaucoma.Extracellular vesicles and circulating nucleic acids · 2024Article
- Distinct Metabolic Profiles of Ocular Hypertensives in Response to Hypoxia.International journal of molecular sciences · 2023Article
- Computational methods in glaucoma research: Current status and future outlook.Molecular aspects of medicine · 2023Review
- Smart Contact Lenses as Wearable Ophthalmic Devices for Disease Monitoring and Health Management.Chemical reviews · 2023Review
- Pharmaceutical Approaches to Normal Tension Glaucoma.Pharmaceuticals (Basel, Switzerland) · 2023Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Normal tension glaucoma (NTG) is a multifactorial optic neuropathy characterized by normal intraocular pressure, progressive retinal ganglion cell (RGC) death, and glaucomatous visual field loss. Recent studies have described the mechanisms underlying the pathogenesis of NTG. In addition to controlling intraocular pressure, neuroprotection and reduction of RGC degeneration may be beneficial therapies for NTG. In this review, we summarized the main regulatory mechanisms of RGC death in NTG, including autophagy, glutamate neurotoxicity, oxidative stress, neuroinflammation, immunity, and vasoconstriction. Autophagy can be induced by retinal hypoxia and axonal damage. In this process, ischemia can cause mutations of optineurin and activate the nuclear factor-kappa B pathway. Glutamate neurotoxicity is induced by the over-stimulation of N-methyl-D-aspartate membrane receptors by glutamate, which occurs in RGCs and induces progressive glaucomatous optic neuropathy. Oxidative stress also participates in NTG-related glaucomatous optic neuropathy. It impairs the mitochondrial and DNA function of RGCs through the apoptosis signal-regulating kinase-JUN N-terminal kinase pathway. Moreover, it increases inflammation and the immune response of RGCs. Endothelin 1 causes endothelial dysfunction and impairment of ocular blood flow, promoting vasospasm and glaucomatous optic neuropathy, as a result of NTG. In conclusion, we discussed research progress on potential options for the protection of RGCs, including TANK binding kinase 1 inhibitors regulating autophagy, N-methyl-D-aspartate receptor antagonists inhibiting glutamate toxicity, ASK1 inhibitors regulating mitochondrial function, and antioxidants inhibiting oxidative stress. In NTG, RGC death is regulated by a network of mechanisms, while various potential targets protect RGCs. Collectively, these findings provide insight into the pathogenesis of NTG and potential therapeutic strategies.
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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.