ArticleAmerican journal of translational research2016
Adeno-associated virus mediated SOD gene therapy protects the retinal ganglion cells from chronic intraocular pressure elevation induced injury via attenuating oxidative stress and improving mitochondrial dysfunction in a rat model.
Article in American journal of translational research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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Who cites it
29 citing papers in PubMed, 41 citations in OpenAlex.
- Experimental upregulation of Lancl1 promotes axon regeneration after optic nerve injury in vivo.Experimental neurology · 2026Article
- A paradoxical relationship between mitochondrial calcium regulation and retinal ganglion cell degeneration after axon damage.bioRxiv : the preprint server for biology · 2026Article
- Research progress on molecular therapy for glaucoma (Review).Molecular medicine reports · 2026Review
- Changes in the Protein Composition of the Aqueous Humor in Patients with Glaucoma: An Update Review.International journal of molecular sciences · 2025Review
- Article
- Gene therapy for glaucoma: Targeting key mechanisms.Vision research · 2024Review
- Advances in Neuroprotection in Glaucoma: Pharmacological Strategies and Emerging Technologies.Pharmaceuticals (Basel, Switzerland) · 2024Review
- AAV-mediated gene therapies for glaucoma and uveitis: are we there yet?Expert reviews in molecular medicine · 2024Review
- Circumlimbal suture and laser burns: Comparison between two different chronic glaucoma models.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024Article
- Potential use of antioxidants for the treatment of chronic inflammatory diseases.Frontiers in pharmacology · 2024Review
- Molecular pathways in experimental glaucoma models.Frontiers in neuroscience · 2024Review
- The concept of gene therapy for glaucoma: the dream that has not come true yet.Neural regeneration research · 2024Review
- Adeno-associated virus mediated gene therapy for neuroprotection of retinal ganglion cells in glaucoma.Vision research · 2023Review
- Label-free LC-MS/MS proteomics analyses reveal proteomic changes in oxidative stress and the SOD antioxidant strategy in TM cells.Clinical proteomics · 2022Article
- Animal Model Contributions to Primary Congenital Glaucoma.Journal of ophthalmology · 2022Review
- Risk Factors for Retinal Ganglion Cell Distress in Glaucoma and Neuroprotective Potential Intervention.International journal of molecular sciences · 2021Review
- The Present and Future of Mitochondrial-Based Therapeutics for Eye Disease.Translational vision science & technology · 2021Article
- Looking into the future: Gene and cell therapies for glaucoma.Veterinary ophthalmology · 2021Review
- Adeno-Associated Viral Vectors in Neuroscience Research.Molecular therapy. Methods & clinical development · 2020Review
- The Relevance of Oxidative Stress in the Pathogenesis and Therapy of Retinal Dystrophies.Antioxidants (Basel, Switzerland) · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeThis study aimed to determine whether chronic intraocular pressure (IOP) elevation induces retinal oxidative stress and alters mitochondrial morphology and function of retinal ganglion cells (RGC) and to explore the effects of AAV-SOD2 gene therapy on the RGC survival and mitochondrial dysfunction.
methodsChronic experimental glaucoma was induced unilaterally in adult male Sprague-Dawley rats by laser burns at trabecular meshwork and episcleral veins 2 times with an interval of one week. One eye of each rat was intravitreally pretreated with recombinant adeno-associated virus expressing SOD2 (AAV-SOD2) or recombinant AAV expressing GFP (AAV-GFP) 21 days before glaucoma induction. RGCs counting, morphometric analysis of retina and optic nerve, and detection of activities of retinal SOD2 and catalase, MDA, mitochondrial morphology, mitochondrial dynamin protein OPA1 and DRP-1 expressions were conducted at 4, 8, 12 and 24 weeks.
resultsSevere RGC loss, degeneration of optic nerve, reduced thickness of RGC layer and nerve fiber layer, significant decrease in total SOD and catalase activities, mitochondrial dysfunction and increased MDA were observed at 4, 8, 12 and 24 weeks after glaucoma. Pretreatment with AAV-SOD2 significantly reduced MDA and attenuated the damage to RGCs through a mitochondria-related pathway.
conclusionAAV mediated pre-treatment with SOD2 is able to attenuate oxidative stress and improve mitochondrial dysfunction of RGC and optic nerve secondary to glaucoma. Thus, SOD2 may be used to prevent the retinal RGCs from glaucoma, which provides a promising strategy for glaucoma therapy.
Indexed as
Identifiers
27158370PMC4846927W2390290940What OpenQuestion holds
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.