ArticlePloS one2016
Autophagy and Mitochondrial Dysfunction in Tenon Fibroblasts from Exfoliation Glaucoma Patients.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.
- Genetic association study of exfoliation syndrome identifies a protective rare variant at LOXL1 and five new susceptibility loci.Nature genetics · 2017Pooled it
- Mitochondrial insufficiencies and neuroprotection in glaucoma.International ophthalmology · 2026Review
- Establishment of an Advanced In Vitro Model for Pseudoexfoliation Syndrome and Glaucoma.Investigative ophthalmology & visual science · 2025Article
- Evaluation of the effect of autophagy on pseudoexfoliation syndrome.The Journal of international medical research · 2025Article
- Mitochondrial and microtubule defects in Exfoliation Glaucoma.Free radical biology & medicine · 2025Article
- New Insights into the Role of Cellular Senescence and Its Therapeutic Implications in Ocular Diseases.Bioengineering (Basel, Switzerland) · 2025Review
- Exosomal microRNA from Plasma in Patients with Pseudoexfoliation Glaucoma of Korea.International journal of molecular sciences · 2025Article
- The Ocular Surface and the Anterior Segment of the Eye in the Pseudoexfoliation Syndrome: A Comprehensive Review.International journal of molecular sciences · 2025Review
- Protein misfolding and mitochondrial dysfunction in glaucoma.Frontiers in cell and developmental biology · 2025Review
- Unfolded proteins and aggregates: The role of proteostasis in pseudoexfoliation pathology.Molecular vision · 2025Review
- Article
- Candidate SNP Markers Significantly Altering the Affinity of the TATA-Binding Protein for the Promoters of Human Genes Associated with Primary Open-Angle Glaucoma.International journal of molecular sciences · 2024Article
- Massively parallel sequencing of mitochondrial genome in primary open angle glaucoma identifies somatically acquired mitochondrial mutations in ocular tissue.Scientific reports · 2024Article
- Rates of retinal nerve fiber layer loss in early-stage pseudoexfoliation and primary open-angle glaucoma patients using optical coherence tomography.International ophthalmology · 2024Article
- 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
- NAD salvage pathway machinery expression in normal and glaucomatous retina and optic nerve.Acta neuropathologica communications · 2023Article
- Proteostasis in aging-associated ocular disease.Molecular aspects of medicine · 2022Review
- Genome-Wide RNA Sequencing of Human Trabecular Meshwork Cells Treated with TGF-β1: Relevance to Pseudoexfoliation Glaucoma.Biomolecules · 2022Article
- Monitoring basal autophagy in the retina utilizing CAG-mRFP-EGFP-MAP1LC3B reporter mouse: technical and biological considerations.Autophagy · 2022Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
purposeTo test the hypothesis that autophagy dysfunction is involved in exfoliation syndrome (XFS), a systemic disorder of extracellular elastic matrices that causes a distinct form of human glaucoma.
methodsFibroblasts derived from tenon tissue discards (TFs) from filtration surgery to relieve intraocular pressure in XFS patients were compared against age-matched TFs derived from surgery in primary open-angle glaucoma (POAG) patients or from strabismus surgery. Differential interference contrast light, and electron microscopy were used to examine structural cell features. Immunocytochemistry was used to visualize LOXL1 and Fibulin-5, lysosomes, endosomes, Golgi, and microtubules. Light scatter, Cyto-IDTM and JC1 flow cytometry were used to measure relative cell size, autophagic flux rate and mitochondrial membrane potential (MMPT), respectively. Enhanced autophagy was induced by serum withdrawal.
resultsIn culture, XFS-TFs were 1.38-fold larger (by light scatter ratio, p = 0.05), proliferated 42% slower (p = 0.026), and were morphologically distinct in 2D and 3D culture compared to their POAG counterparts. In extended 3D cultures, XFS-TFs accumulated 8-10 times more Fibulin-5 than the POAG-TFs, and upon serum withdrawal, there were marked deficiencies in relocation of endosomes and lysosomes to the perinuclear area. Correspondingly, the XFS-TFs displayed significant accumulation of the autophagasome marker LC3 II (3.9 fold increase compared to POAG levels, p = 0.0001) and autophagic flux rate as measured by Cyto-ID dye was 53% lower in XFS-TFs than in POAG-TFs (p = 0.01), indicating reduced clearance of autophagasomes. Finally the percent of cells with diminished MMPT was 3-8 times larger in the XFS-TFs than in POAG-TFs (p = 0.02).
conclusionsOur results provide for the first time a link between XFS pathology to autophagy dysfunction, a major contributor to multiple age related diseases systemically throughout the body, in the brain and in the retina. A diminished capacity for degradation of denatured protein and aging cellular organelles may underpin the development of extracellular protein aggregates in XFS.
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