ArticleJournal of neuroinflammation2014
Tumor necrosis factor alpha has an early protective effect on retinal ganglion cells after optic nerve crush.
Article in Journal of neuroinflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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.
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Who cites it
39 citing papers in PubMed, 57 citations in OpenAlex.
- Dual role of microglia in glaucoma: Regulation of neuroinflammation and neuroregeneration.Neural regeneration research · 2026Article
- Glaucoma and Autoimmunity: Immunopathogenic Mechanisms and Emerging Immunomodulatory Therapies.Biomedicines · 2026Review
- IL-1-mediated vitreous inflammation as an early indicator of retinal ganglion cell loss following acute optic nerve injury.Journal of neuroinflammation · 2026Article
- IL1A enhances TNF-induced retinal ganglion cell death.Frontiers in aging neuroscience · 2026Article
- Vitreous Inflammation as an Early Indicator of Retinal Ganglion Cell Loss Following Acute Optic Nerve Injury in Mice.bioRxiv : the preprint server for biology · 2025Article
- Functional significance of commonly regulated genes in mechanically and chemically induced retinal ganglion cell death in rat eyes.Scientific reports · 2025Article
- Immunomodulatory, Antioxidant, and Potential Anticancer Activity of the Polysaccharides of the FungusMolecules (Basel, Switzerland) · 2024Article
- Assessment of Brain-Derived Neurotrophic Factor on Retinal Structure and Visual Function in Rodent Models of Optic Nerve Crush.Pharmaceuticals (Basel, Switzerland) · 2024Article
- The Role of Complement Dysregulation in Glaucoma.International journal of molecular sciences · 2024Review
- A peptide mimic of SOCS1 modulates equine peripheral immune cellsFrontiers in immunology · 2024Article
- Contralateral Astrocyte Response to Acute Optic Nerve Damage Is Mitigated by PANX1 Channel Activity.International journal of molecular sciences · 2023Article
- Azithromycin and Sildenafil May Have Protective Effects on Retinal Ganglion Cells via Different Pathways: Study in a Rodent Microbead Model.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Neuroprotective Effect of Azithromycin Following Induction of Optic Nerve Crush in Wild Type and Immunodeficient Mice.International journal of molecular sciences · 2022Article
- Inhibition of Heat Shock Protein B8 Alleviates Retinal Dysfunction and Ganglion Cells Loss Via Autophagy Suppression in Mouse Axonal Damage.Investigative ophthalmology & visual science · 2022Article
- Harnessing the Neuroprotective Behaviors of Müller Glia for Retinal Repair.Frontiers in bioscience (Landmark edition) · 2022Review
- Retinal Glutamate Neurotransmission: From Physiology to Pathophysiological Mechanisms of Retinal Ganglion Cell Degeneration.Life (Basel, Switzerland) · 2022Review
- Proteome alterations in the aqueous humor reflect structural and functional phenotypes in patients with advanced normal-tension glaucoma.Scientific reports · 2022Article
- Targeting Differential Roles of Tumor Necrosis Factor Receptors as a Therapeutic Strategy for Glaucoma.Frontiers in immunology · 2022Review
- Role of glia in optic nerve.Progress in retinal and eye research · 2021Review
- Correlation of NUCB2/Nesfatin-1 with Cytokine Levels in Primary Open-Angle Glaucoma.Clinical ophthalmology (Auckland, N.Z.) · 2021Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundGlaucoma is an optic neuropathy that is characterized by the loss of retinal ganglion cells (RGCs) initiated by damage to axons in the optic nerve. The degeneration and death of RGCs has been thought to occur in two waves. The first is axogenic, caused by direct insult to the axon. The second is somatic, and is thought to be caused by the production of inflammatory cytokines from the activated retinal innate immune cells. One of the cytokines consistently linked to glaucoma and RGC damage has been TNFα. Despite strong evidence implicating this protein in neurodegeneration, a direct injection of TNFα does not mimic the rapid loss of RGCs observed after acute optic nerve trauma or exposure to excitotoxins. This suggests that our understanding of TNFα signaling is incomplete.
methodsRGC death was induced by optic nerve crush in mice. The role of TNFα in this process was examined by quantitative PCR of Tnfα gene expression, and quantification of cell loss in Tnfα (-/-) mice or in wild-type animals receiving an intraocular injection of exongenous TNFα either before or after crush. Signaling pathways downstream of TNFα were examined by immunolabeling for JUN protein accumulation or activation of EGFP expression in NFκB reporter mice.
resultsOptic nerve crush caused a modest increase in Tnfα gene expression, with kinetics similar to the activation of both macroglia and microglia. A pre-injection of TNFα attenuated ganglion cell loss after crush, while ganglion cell loss was more severe in Tnfα (-/-) mice. Conversely, over the long term, a single exposure to TNFα induced extrinsic apoptosis in RGCs. Müller cells responded to exogenous TNFα by accumulating JUN and activating NFκB.
conclusionEarly after optic nerve crush, TNFα appears to have a protective role for RGCs, which may be mediated through Müller cells.
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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.