ArticleClinical ophthalmology (Auckland, N.Z.)2021
Switch to Autophagy the Key Mechanism for Trabecular Meshwork Death in Severe Glaucoma.
Article in Clinical ophthalmology (Auckland, N.Z.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 12 citations in OpenAlex.
- Digoxin Attenuates Ocular Hypertension and Protects Trabecular Meshwork Cells via Ferroptosis Inhibition.Investigative ophthalmology & visual science · 2026Article
- Epigenetics of glaucoma in the trabecular meshwork.Clinical epigenetics · 2025Review
- Exploring diagnostic m6A regulators in primary open-angle glaucoma: insight from gene signature and possible mechanisms by which key genes function.BMC medical genomics · 2025Article
- Integrated Proteomics and Protein Co-expression Network Analysis Identifies Novel Epileptogenic Mechanism in Mesial Temporal Lobe Epilepsy.Molecular neurobiology · 2024Article
- Article
- Genome-wide RNA sequencing of ocular fibroblasts from glaucomatous and normal eyes: Implications for glaucoma management.PloS one · 2024Article
- A Feedback Loop between TGF-β1 andCurrent issues in molecular biology · 2023Article
- m6A Modification-Association with Oxidative Stress and Implications on Eye Diseases.Antioxidants (Basel, Switzerland) · 2023Review
- Alternate Causes for Pathogenesis of Exfoliation Glaucoma, a Multifactorial Elastotic Disorder: A Literature Review.Current issues in molecular biology · 2022Review
- Multiomics analysis reveals the mechanical stress-dependent changes in trabecular meshwork cytoskeletal-extracellular matrix interactions.Frontiers in cell and developmental biology · 2022Article
- Global and Comparative Proteome Signatures in the Lens Capsule, Trabecular Meshwork, and Iris of Patients With Pseudoexfoliation Glaucoma.Frontiers in molecular biosciences · 2022Article
- Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeThe key differences in cell death mechanisms in the trabecular meshwork (TM) in adult moderate and severe primary glaucoma remain still unanswered. This study explored key differences in cell death mechanisms in the trabecular meshwork (TM) in adult moderate and severe primary glaucoma.
designIn-vitro laboratory study on surgical specimens and primary cell lines.
methodsSelect cell death-related proteins differentially expressed on mass spectrometric analysis in ex-vivo dissected TM specimens patients with severe adult primary open-angle (POAG) or angle-closure glaucoma (PACG) compared to controls (cadaver donor cornea) were validated for temporal changes in cell death-related gene expression on in-vitro primary human TM cell culture after 48 hours (moderate) or 72 hours (severe) oxidative stress with H
resultsAutophagy-related proteins seemed to be the predominant cell-death mechanism over apoptosis in ex-vivo dissected TM specimens in severe glaucoma. Analyzing HTM cell gene expression at 48 hours and 72 hours of oxidative stress, autophagy genes were up-regulated at 48-72 hours of exposure in contrast to apoptosis-related genes, showing down-regulation at 72 hours. There was associated increased expression of H3K14ac in HTM after 72 hours of oxidative stress and in peripheral blood of severe POAG and PACG.
conclusionA preference of autophagy over apoptosis may underlie stage transition from moderate to severe glaucoma in the trabecular meshwork or peripheral blood, which may be tightly regulated by epigenetic modulators.
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