ArticleCell death & disease2022
Age-related visual impairments and retinal ganglion cells axonal degeneration in a mouse model harboring OPTN (E50K) mutation.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Sensory decline in aging and neurodegeneration: A mitochondrial perspective.Pharmacological research · 2026Review
- The mitochondria-targeted peptide HDAP2 reduces mitochondrial loss and retinal ganglion cell degeneration after optic nerve injury.Neuroscience · 2026Article
- Chitosan-rapamycin carbon dots rejuvenate autologous Sca-1⁺ stem cells paracrine function for neuroprotection in normal tension glaucoma.Stem cell research & therapy · 2026Article
- Single-Cell Transcriptome Analysis of the Retina During the Development of Normal Tension Glaucoma in Mice.Inflammation · 2025Article
- Microglia Drive Peripapillary Vascular Density Reduction in Normal Tension Glaucoma by Regulating the Rpl17/Stat5b/Apoa1 Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Inhibiting NLRP3 Inflammasome Activation to Alleviate Retinal Inflammation and Protect the Optic Nerve of OPTN(E50K)Mice.Inflammation · 2025Article
- Oral 7,8-Dihydroxyflavone Protects Retinal Ganglion Cells by Modulating the Gut-Retina Axis and Inhibiting Ferroptosis via the Indoleacrylic Acid-AhR-ALDH1A3-FSP1 Pathway.CNS neuroscience & therapeutics · 2025Article
- RIP1 inhibition protects retinal ganglion cells in glaucoma models of ocular injury.Cell death and differentiation · 2025Article
- Revealing the role of regulatory microglial IRF7-NLRP3 interactions in optic nerve damage of normal-tension glaucoma based on single-cell RNA sequencing.Frontiers in immunology · 2025Article
- Hidden Markov models reveal behavioral state dynamics in depth-related locomotion in mice.PloS one · 2025Article
- Axonopathy Underlying Amyotrophic Lateral Sclerosis: Unraveling Complex Pathways and Therapeutic Insights.Neuroscience bulletin · 2024Review
- Chitosan-Rapamycin Carbon Dots Alleviate Glaucomatous Retinal Injury by Inducing Autophagy to Promote M2 Microglial Polarization.International journal of nanomedicine · 2024Article
- Endoplasmic reticulum stress: molecular mechanism and therapeutic targets.Signal transduction and targeted therapy · 2023Review
- Elevated Intraocular Pressure and Glaucomatous Optic Neuropathy: Genes to Disease Mechanisms, Therapeutic Drugs, and Gene Therapies.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Generation of iPSC-derived human forebrain organoids assembling bilateral eye primordia.Nature protocols · 2023Review
- Autophagy in the retinal neurovascular unit: New perspectives into diabetic retinopathy.Journal of diabetes · 2023Review
- Analysis of risk and protective factors associated with retinal nerve fiber layer defect in a Chinese adult population.International journal of ophthalmology · 2023Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Retinal ganglion cells (RGCs) axons are the signal carriers of visual information between retina and brain. Therefore, they play one of the important roles affected in many optic neurodegenerative diseases like glaucoma. Among the genetic risks associated with glaucoma, the E50K mutation in the Optineurin (OPTN) gene are known to result in glaucoma in the absence of increased intraocular pressure (IOP), whereas the relevant pathological mechanism and neurological issues remain to be further investigated. In this study, the OPTN (E50K) mutant mouse model was established through CRISPR/Cas9-mediated genome editing, and aging-related RGCs loss and the visual dysfunction were identified. In E50K mice 16 months old, the axonal transport decreased comparing to wild-type (WT) mice at the same age. Furthermore, results of electron microscopy demonstrated significant morphological anomaly of mitochondria in RGCs axons of young E50K mice 3 months old, and these changes were aggravated with age. These indicated that the damaged mitochondria-associated dysfunction of RGCs axon should play an etiological role in glaucoma as an age-related outcome of OPTN (E50K) mutation. The findings of this study have potential implications for the targeted prevention and treatment of NTG.
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