ArticleMedical science monitor basic research2020
Metformin Prevents H₂O₂-Induced Senescence in Human Lens Epithelial B3 Cells.
Article in Medical science monitor basic research, 2020. 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.
- Cellular Senescence of Lens Epithelial Cells and Age-Related Cataract: A Systematic Review.Bioengineering (Basel, Switzerland) · 2026Review
- Lens epithelial cells senescence in cataract pathogenesis and emerging therapeutic opportunities.Frontiers in cell and developmental biology · 2026Review
- Aging of the human eye lens: Epigenetic landscape and therapeutic targets in age‑related cataracts (Review).International journal of molecular medicine · 2025Review
- Klotho relieves HInternational ophthalmology · 2024Article
- Co-Delivery of Valsartan and Metformin from a Thermosensitive Hydrogel-Nanoparticle System Promotes Collagen Production in Proliferating and Senescent Primary Human Dermal Fibroblasts.Biomacromolecules · 2024Article
- 7-Ketocholesterol accelerates pancreatic β-cell senescence by inhibiting the SIRT1/CDK4-Rb-E2F1 signaling pathway.Islets · 2023Article
- Senopathies-Diseases Associated with Cellular Senescence.Biomolecules · 2023Article
- Astragalus polysaccharide alleviated hepatocyte senescence via autophagy pathway.The Kaohsiung journal of medical sciences · 2022Article
- Geroscience-guided repurposing of FDA-approved drugs to target aging: A proposed process and prioritization.Aging cell · 2022Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND The primary purpose of this study was to investigate the protective effect of metformin against hydrogen peroxide (H₂O₂)-induced cellular senescence and to explore the underlying molecular mechanism of lens epithelial cell senescence. MATERIAL AND METHODS We used H₂O₂ to establish senescence in human lens epithelial B3 cells. The cells were exposed to H₂O₂ for different numbers of days to mimic aging. Senescence was assessed by senescence-associated ß-galactosidase staining, and the molecular mechanism was assessed by real-time polymerase chain reaction (RT-PCR) and western blot analysis. The cultured cells were exposed to 150 μM H₂O₂ for 7 days with or without metformin to detect the underlying molecular mechanism of lens epithelial cell senescence. RESULTS The lens epithelial cells exposed to 150 µM H₂O₂ for 7 days exhibited senescence. The expression levels of senescence-related markers were increased in H₂O₂-treated cells. Metformin prevented H₂O₂-induced cellular senescence in human lens epithelial B3 cells. CONCLUSIONS These findings suggest that senescence marker expression is increased in the cells exposed to H₂O₂. Metformin protects human lens epithelial B3 cells from H₂O₂-induced senescence.
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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.