ArticleJournal of neuroinflammation2021
Soluble tumor necrosis factor-alpha-induced hyperexcitability contributes to retinal ganglion cell apoptosis by enhancing Nav1.6 in experimental glaucoma.
Article in Journal of neuroinflammation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 47 citations in OpenAlex.
- Voltage-gated sodium channels in the nervous system: Molecular physiology to therapeutic interventions.Neural regeneration research · 2026Article
- IL-1β-mediated interaction between Müller cells and microglia through CXCL1/5-CXCR2 aggravates visual dysfunction in experimental glaucoma.Journal of neuroinflammation · 2026Article
- Article
- Experimental models to study oxidative stress in glaucoma: integratingFrontiers in pharmacology · 2026Review
- Tumor Necrosis Factor Alpha-Mediated Interaction Between Microglia and Müller Cells Exacerbates Retinal Ganglion Cell Damage in Experimental Glaucoma.Neuroscience bulletin · 2026Article
- TNF-α-preconditioning enhances analgesic efficacy of mesenchymal stem cell-derived extracellular vesicle in neuropathic painBioactive materials · 2025Article
- Identification of diagnostic biomarkers and dissecting immune microenvironment with crosstalk genes in the POAG and COVID-19 nexus.Scientific reports · 2025Article
- Exosomal TNF-α mediates voltage-gated Na+ channel 1.6 overexpression and contributes to brain tumor-induced neuronal hyperexcitability.The Journal of clinical investigation · 2024Article
- Apoptosis in glaucoma: A new direction for the treatment of glaucoma (Review).Molecular medicine reports · 2024Review
- Trigeminal Postherpetic Neuralgia: From Pathophysiology to Treatment.Current pain and headache reports · 2024Review
- NLRP3 and autophagy in retinal ganglion cell inflammation in age-related macular degeneration: potential therapeutic implications.International journal of ophthalmology · 2024Review
- TNFR1 signaling converging on FGF14 controls neuronal hyperactivity and sickness behavior in experimental cerebral malaria.Journal of neuroinflammation · 2023Article
- Therapeutic strategies for glaucoma and optic neuropathies.Molecular aspects of medicine · 2023Review
- L- and T-type CaNeural regeneration research · 2023Article
- Role of the voltage‑gated sodium channel Nav1.6 in glioma and candidate drugs screening.International journal of molecular medicine · 2023Article
- Microglia-derived TNF-α contributes to RVLM neuronal mitochondrial dysfunction via blocking the AMPK-Sirt3 pathway in stress-induced hypertension.Journal of neuroinflammation · 2023Article
- Activation of Endothelial Large Conductance Potassium Channels Protects against TNF-α-Induced Inflammation.International journal of molecular sciences · 2023Article
- Factors Associated with Elevated Tumor Necrosis Factor-α in Aqueous Humor of Patients with Open-Angle Glaucoma.Journal of clinical medicine · 2022Article
- Sensitization of colonic nociceptors by TNFα is dependent on TNFR1 expression and p38 MAPK activity.The Journal of physiology · 2022Article
- Erythropoietin in Optic Neuropathies: Current Future Strategies for Optic Nerve Protection and Repair.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundNeuroinflammation plays an important role in the pathogenesis of glaucoma. Tumor necrosis factor-alpha (TNF-α) is a major pro-inflammatory cytokine released from activated retinal glial cells in glaucoma. Here, we investigated how TNF-α induces retinal ganglion cell (RGC) hyperexcitability and injury.
methodsWhole-cell patch-clamp techniques were performed to explore changes in spontaneous firing and evoked action potentials, and Na
resultsIntravitreal injection of soluble TNF-α significantly increased the spontaneous firing frequencies of RGCs in retinal slices. When the synaptic transmissions were blocked, more than 90% of RGCs still showed spontaneous firing; both the percentage of cells and firing frequency were higher than the controls. Furthermore, the frequency of evoked action potentials was also higher than the controls. Co-injection of the TNF-α receptor 1 (TNFR1) inhibitor R7050 eliminated the TNF-α-induced effects, suggesting that TNF-α may directly act on RGCs to induce cell hyperexcitability through activating TNFR1. In RGCs acutely isolated from TNF-α-injected retinas, Na
conclusionsTNF-α/TNFR1 signaling induces RGC hyperexcitability by selectively upregulating Nav1.6 Na
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Registered trials
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