ArticleBMC ophthalmology2016
Oxidative stress and premature senescence in corneal endothelium following penetrating keratoplasty in an animal model.
Article in BMC ophthalmology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 19 citations in OpenAlex.
- Pathological Interplay of ROS With Myofibroblasts: An Impediment to Corneal Restitution.Oxidative medicine and cellular longevity · 2026Review
- Corneal oxidative stress, inflammation, and senescence as key drivers of ocular pathology in a chronic graft-versus-host disease model.BMC ophthalmology · 2025Article
- Cellular senescence and ophthalmic diseases: narrative review.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2023Review
- A p-Tyr42 RhoA Inhibitor Promotes the Regeneration of Human Corneal Endothelial Cells by Ameliorating Cellular Senescence.Antioxidants (Basel, Switzerland) · 2023Article
- Solubilized ubiquinol for preserving corneal function.Biomaterials · 2021Article
- Tumor necrosis factor-alpha and interferon-gamma induce inflammasome-mediated corneal endothelial cell death.Experimental eye research · 2021Article
- Transplantation of human induced pluripotent stem cell-derived neural crest cells for corneal endothelial regeneration.Stem cell research & therapy · 2021Article
- D-Galactose-induced oxidative stress and mitochondrial dysfunction in the cochlear basilar membrane: an in vitro aging model.Biogerontology · 2020Article
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Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe purpose of this study was to address the question of how the premature senescence process may affect corneal endothelium after penetrating keratoplasty, because the quality of donor corneal endothelial cells is important for corneal transplant success.
methodsThe cell senescence and induced oxidative stress in corneal endothelium were assessed using a normal-risk orthotopic mice corneal transplantation model. Senescence associated beta-galactosidase (SA-beta-Gal) staining was used to evaluate premature senescence in the endothelium of corneal allografts. Oxidative Stress and Antioxidant Defense RT(2)-PCR Arrays and in vitro experimental model using H2O2 treatment were used to investigate the possible mechanism.
resultsSA-beta-Gal positivity was observed obviously in mice corneal endothelium of allogenic group and the levels of p16(INK4a) message and protein increased in endothelium of allogenic group compared to syngenic group. By PCR array, an oxidant-antioxidant imbalance was found in the endothelium of corneal allograft after PKP. The results from mice model were validated using human endothelium samples of corneal allograft after PKP. We also developed an in vitro experimental model using H2O2 treatment to simulate a state of oxidative stress in cultured human corneal endothelial cells (HCECs) and found that elevated ROS levels, the up-regulation of CDK inhibitors and ROS-mediated p16(INK4A) up-regulation in HCECs occur via the ASK1-p38 MAPK pathway.
conclusionsOur results demonstrate the presence of oxidative stress and premature senescence in the endothelium of corneal allografts following PKP.
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