ArticleScientific reports2024
Ripa-56 protects retinal ganglion cells in glutamate-induced retinal excitotoxic model of glaucoma.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 12 citations in OpenAlex.
- Mitochondrial Homeostasis Mediates the Sustained Neuroprotection of CNTF-Chitosan Hydrogel Against NMDA-Induced Retinal Ganglion Cell Excitotoxicity.International journal of molecular sciences · 2026Article
- Neurotoxic effects of dietary glutamate in glaucoma and potential nutritional and pharmacological therapies: a scoping review.International ophthalmology · 2026Article
- The Wnt/StarD7 axis protects retinal ganglion cells from glutamate excitotoxicity by inhibiting ferroptosis.Biology direct · 2026Article
- Probing Allosteric Kinase Modulators as Next Game-Changers in Fighting Neurodegeneration.Journal of medicinal chemistry · 2026Review
- Glycosylation-driven necroptosis in retinal degeneration: dual rescue by AAV8 gene therapy and RIPK1 inhibition.Cell death discovery · 2026Article
- Overexpression or Activation of Potassium Channel TASK-3 Protects Retinal Ganglion Cells and Restores Visual Function in Optic Nerve Crush.Investigative ophthalmology & visual science · 2026Article
- Research Advances in Glanimal Models of Glaucoma: Exploring Multidimensional Mechanisms and Novel Therapeutic Strategies.Pharmaceutics · 2026Review
- Emerging Roles of Regulated Cell Death-mediated Inflammation in Pathophysiology of Ocular Diseases.Journal of ophthalmic & vision research · 2026Review
- Ferroptosis and retinal ganglion cell death in glaucoma: Mechanisms and therapeutic approaches.Journal of pharmaceutical analysis · 2026Review
- Neuroprotective and intraocular pressure lowering effects of dual-functional memantine nitrate MN-08 on the experimental models of glaucoma.Scientific reports · 2025Article
- ENO1 Dysfunction-Mediated Glycolytic Attenuation Exacerbates Oxidative Stress-Induced Retinal Ganglion Cell Death via Altered ATP Synthesis Pathway.Investigative ophthalmology & visual science · 2025Article
- Ferroptosis Contributes to Retinal Ganglion Cell Loss in GLAST Knockout Mouse Model of Normal Tension Glaucoma.Investigative ophthalmology & visual science · 2025Article
- The molecular mechanisms underlying retinal ganglion cell apoptosis and optic nerve regeneration in glaucoma (Review).International journal of molecular medicine · 2025Review
- Translational Research and Therapies for Neuroprotection and Regeneration of the Optic Nerve and Retina: A Narrative Review.International journal of molecular sciences · 2024Review
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
Glaucoma is a prevalent cause of blindness globally, characterized by the progressive degeneration of retinal ganglion cells (RGCs). Among various factors, glutamate excitotoxicity stands out as a significant contributor of RGCs loss in glaucoma. Our study focused on Ripa-56 and its protective effect against NMDA-induced retinal damage in mice, aiming to delve into the potential underlying mechanism. The R28 cells were categorized into four groups: glutamate (Glu), Glu + Ripa-56, Ripa-56 and Control group. After 24 h of treatment, cell death was assessed by PI / Hoechst staining. Mitochondrial membrane potential changes, apoptosis and reactive oxygen species (ROS) production were analyzed using flow cytometry. The alterations in the expression of RIP-1, p-MLKL, Bcl-2, BAX, Caspase-3, Gpx4 and SLC7A11 were examined using western blot analysis. C57BL/6j mice were randomly divided into NMDA, NMDA + Ripa-56, Ripa-56 and control groups. Histological changes in the retina were evaluated using hematoxylin and eosin (H&E) staining. RGCs survival and the protein expression changes of RIP-1, Caspase-3, Bcl-2, Gpx4 and SLC7A11 were observed using immunofluorescence. Ripa-56 exhibited a significant reduction in the levels of RIP-1, p-MLKL, Caspase-3, and BAX induced by glutamate, while promoting the expression of Bcl-2, Gpx-4, and SLC7A1 in the Ripa-56-treated group. In our study, using an NMDA-induced normal tension glaucoma mice model, we employed immunofluorescence and H&E staining to observe that Ripa-56 treatment effectively ameliorated retinal ganglion cell loss, mitigating the decrease in retinal ganglion cell layer and bipolar cell layer thickness caused by NMDA. In this study, we have observed that Ripa-56 possesses remarkable anti- necroptotic, anti-apoptotic and anti-ferroptosis properties. It demonstrates the ability to combat not only glutamate-induced excitotoxicity in R28 cells, but also NMDA-induced retinal excitotoxicity in mice. Therefore, Ripa-56 could be used as a potential retinal protective agent.
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