ArticleJournal of cellular and molecular medicine2021
Metformin alleviates oxidative stress-induced senescence of human lens epithelial cells via AMPK activation and autophagic flux restoration.
Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 40 citations in OpenAlex.
- Biliverdin Reductase A Protects Lens Epithelial Cells against Oxidative Damage and Cellular Senescence in Age-Related Cataract.Oxidative medicine and cellular longevity · 2022Trial
- Review
- Cellular Senescence of Lens Epithelial Cells and Age-Related Cataract: A Systematic Review.Bioengineering (Basel, Switzerland) · 2026Review
- Aging, oxidative stress, and cataracts: Therapeutic prospects and translational insights into peroxiredoxin 6.Progress in retinal and eye research · 2026Review
- Lens epithelial cells senescence in cataract pathogenesis and emerging therapeutic opportunities.Frontiers in cell and developmental biology · 2026Review
- Metformin attenuates TBHP-induced oxidative injury in human lens epithelial cells and is associated with SIRT1/FOXO1-related autophagy.PloS one · 2026Article
- Targeting Aging and Diseases Associated with Ferroptosis and Senescence Through Modulation of Iron, Oxidative Stress and Lipid Peroxidation.Antioxidants (Basel, Switzerland) · 2025Review
- Mitochondrial dysfunction in cellular senescence: a bridge to neurodegenerative disease.npj aging · 2025Review
- Pharmacological Strategies for Cataract Management: From Molecular Targets to Clinical Translation.International journal of molecular sciences · 2025Review
- [Regulatory Role of the AKT1/AMPK Pathway in Oxidative Stress of Lens Epithelial Cells in Cataract Patients].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2025Article
- Enhancing immunity during ageing by targeting interactions within the tissue environment.Nature reviews. Drug discovery · 2025Review
- Effect of metformin on the level of aqueous humor inflammatory cytokines in patients with cataract.Scientific reports · 2025Article
- METTL3-mediated m6A modification of SIRT1 mRNA affects the progression of diabetic cataracts through cellular autophagy and senescence.Journal of translational medicine · 2024Article
- Investigating the Effects of Chelidonic Acid on Oxidative Stress-Induced Premature Cellular Senescence in Human Skin Fibroblast Cells.Life (Basel, Switzerland) · 2024Article
- Oxidative Stress and Cataract Formation: Evaluating the Efficacy of Antioxidant Therapies.Biomolecules · 2024Review
- Metformin rejuvenates Nap1l2-impaired immunomodulation of bone marrow mesenchymal stem cells via metabolic reprogramming.Cell proliferation · 2024Article
- Underlying Mechanisms and Treatment of Cellular Senescence-Induced Biological Barrier Interruption and Related Diseases.Aging and disease · 2024Review
- Article
- A bibliometric and visualized analysis of the pathogenesis of cataracts from 1999 to 2023.Heliyon · 2024Article
- Metformin protects human lens epithelial cells from high glucose-induced senescence and autophagy inhibition by upregulating SIRT1.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2024Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cataracts are the leading cause of blindness worldwide owing to the increasing proportion of elderly individuals in the population. The purpose of this study was to investigate whether metformin could alleviate the occurrence and development of age-related cataract (ARC) and the underlying mechanism. In the present study, we established a senescence model induced by oxidative stress, which was confirmed by measuring β-galactosidase activity, qRT-PCR and Western blotting. In addition, we showed that metformin alleviated the oxidative stress-induced senescence of HLE-B3 cells via the activation of AMPK. Next, we provided evidence that oxidative stress impaired autophagic flux and induced lysosomal dysfunction. Subsequently, we found that metformin restored autophagic flux that had been impaired by oxidative stress by activating AMPK. Additionally, we found that metformin suppressed HLE-B3 cell senescence by improving lysosomal function and inactivating mTOR. Furthermore, the inactivation of AMPK, impairment of autophagic flux and lysosomal dysfunction were observed in the human lens epithelium of ARC. In summary, our data suggest that the activation of AMPK may be a potential strategy for preventing ARC, and metformin may be an emerging candidate to alleviate the formation and development of ARC.
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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.