ArticleInvestigative ophthalmology & visual science2026
Oxidative Stress-Induced Age-Related Bullous Keratopathy in Corneal Endothelial Cells With Lipid Droplets and Vacuoles.
Article in Investigative ophthalmology & visual science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Purpose: We previously demonstrated that intracellular oxidative stress reduces corneal endothelial cells in Tet-mev-1 mice that genetically overproduce mitochondrial superoxide anions. This study aimed to elucidate the physiological processes underlying oxidative stress-induced corneal endothelial cell loss. Methods: Primary cultures of mouse corneal endothelial cells were established. Intracellular lipid droplets were detected using Lipi-Green, and autophagosomes in live cells were visualized using DAPGreen. Autophagy was assessed by immunostaining and Western blot analysis using microtubule-associated protein 1 light chain 3 (LC3). Furthermore, autophagic flux was evaluated by LC3 and p62/SQSTM1 levels with bafilomycin A1. DNA damage was assessed by γH2AX pSer139 immunostaining. Results: Corneal endothelial cells formed a paving stone-like monolayer and expressed endothelial markers. Tet-mev-1 cells, which were mitochondrial oxidative stress-overproduced mouse cells, exhibited senescent-like cells with abnormal lipid droplet accumulation, vacuolation, and DNA damage compared with wild-type cells. Quantitative analyses confirmed increased lipid droplets, autophagosomes, DNA damage, and vacuolated cells. In young Tet-mev-1 cells, autophagy-related responses were relatively preserved under oxidative stress conditions. In contrast, aged Tet-mev-1 cells showed attenuated responses to lysosomal inhibition, suggesting a decline in autophagic degradation capacity with premature aging by oxidative stress. Conclusions: Intracellular oxidative stress is associated with enhanced autophagic activity in young corneal endothelial cells, whereas progressive endothelial cell loss with aging is accompanied by alterations in autophagy-related processes. This shift contributes to the accumulation of lipid droplets, vacuolations, and DNA damage. These findings suggest that maintenance of lipid homeostasis through autophagy-related pathways may play an important role in delaying age-related corneal endothelial dysfunction.
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