ArticleThe Journal of clinical investigation2011
Reduction of ER stress via a chemical chaperone prevents disease phenotypes in a mouse model of primary open angle glaucoma.
Article in The Journal of clinical investigation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 203 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
203 citing papers in PubMed, 278 citations in OpenAlex.
- 4-phenylbutyric acid-loaded mesoporous silica nanoparticles alleviate endoplasmic reticulum stress and reduce intraocular pressure in glaucoma model.Biology direct · 2026Article
- Association between probiotic prescriptions and the incidence of primary open-angle glaucoma in patients with documented dry eye.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2026Article
- Intraocular pressure induced blood retinal barrier compromise in mouse models and human glaucoma.Nature communications · 2026Article
- The Role of Viral Infection and Microbial Dysbiosis in Glaucoma: From Pathogenesis to Therapeutic Strategies.Viruses · 2026Review
- Disease modeling of myocilin mutation-dependent normal tension glaucoma: human retinal ganglion cell susceptibility to unfolded protein response and mTOR signaling.Stem cells (Dayton, Ohio) · 2026Article
- Lipid-nanoparticle-mediated base editing of the trabecular meshwork rescues glaucoma in vivo.JCI insight · 2026Article
- AAV-DJ-Mediated MYOC Silencing as a Gene Therapy Approach for Myocilin-Associated Glaucoma.Investigative ophthalmology & visual science · 2026Article
- Genetic Architecture and Clinical Phenotypes of Primary Open-Angle Glaucoma: An Updated Review of Mendelian Genes, GWAS Loci, and Polygenic Risk.Clinical ophthalmology (Auckland, N.Z.) · 2026Review
- Experimental models to study oxidative stress in glaucoma: integratingFrontiers in pharmacology · 2026Review
- Gene Therapy for Inherited Retinal Disease: Current Strategies, Personalized Medicine, and Future Implications-A Comprehensive Review.Journal of personalized medicine · 2025Review
- Therapeutic mRNA delivery of CRISPR-Cas9 to the trabecular meshwork reverses ocular hypertension in myocilin glaucoma.Molecular therapy. Methods & clinical development · 2025Article
- iPSC-derived ITGA6-positive cells restore aqueous humor outflow in glaucoma eyes.Nature communications · 2025Article
- Rodent Models of Glaucoma: How Mice and Rats Can Help Human Vision Move Out of the Woods and Into the Light.Cells · 2025Review
- Absence of Glaucoma in Tg-MYOCY437H Mice of Diverse Genetic Backgrounds.Investigative ophthalmology & visual science · 2025Article
- Article
- Global research trends on endoplasmic reticulum stress in retinal diseases from 2000 to 2024.International ophthalmology · 2025Review
- Does Age Modify the Relation Between Genetic Predisposition to Glaucoma and Various Glaucoma Traits in the UK Biobank?Investigative ophthalmology & visual science · 2025Article
- Impaired axonal transport contributes to neurodegeneration in a Cre-inducible mouse model of myocilin-associated glaucoma.JCI insight · 2025Article
- Protein misfolding and mitochondrial dysfunction in glaucoma.Frontiers in cell and developmental biology · 2025Review
- Extracellular vesicles as emerging players in glaucoma: Mechanisms, biomarkers, and therapeutic targets.Vision research · 2025Review
143 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
11 authors at 5 institutions in 1 country.
Funding
Abstract
Mutations in myocilin (MYOC) are the most common genetic cause of primary open angle glaucoma (POAG), but the mechanisms underlying MYOC-associated glaucoma are not fully understood. Here, we report the development of a transgenic mouse model of POAG caused by the Y437H MYOC mutation; the mice are referred to herein as Tg-MYOC(Y437H) mice. Analysis of adult Tg-MYOC(Y437H) mice, which we showed express human MYOC containing the Y437H mutation within relevant eye tissues, revealed that they display glaucoma phenotypes (i.e., elevated intraocular pressure [IOP], retinal ganglion cell death, and axonal degeneration) closely resembling those seen in patients with POAG caused by the Y437H MYOC mutation. Mutant myocilin was not secreted into the aqueous humor but accumulated in the ER of the trabecular meshwork (TM), thereby inducing ER stress in the TM of Tg-MYOC(Y437H) mice. Furthermore, chronic and persistent ER stress was found to be associated with TM cell death and elevation of IOP in Tg-MYOC(Y437H) mice. Reduction of ER stress with a chemical chaperone, phenylbutyric acid (PBA), prevented glaucoma phenotypes in Tg-MYOC(Y437H) mice by promoting the secretion of mutant myocilin in the aqueous humor and by decreasing intracellular accumulation of myocilin in the ER, thus preventing TM cell death. These results demonstrate that ER stress is linked to the pathogenesis of POAG and may be a target for treatment in human patients.
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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.