ArticleInvestigative ophthalmology & visual science2021
Aged Nrf2-Null Mice Develop All Major Types of Age-Related Cataracts.
Article in Investigative ophthalmology & visual science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 20 citations in OpenAlex.
- Targeting of Nuclear Factor Erythroid 2-Related Factor 2 (NRF2) Signaling Pathway in Age-Related Eye Diseases: Molecular Mechanisms and Opportunities for therapy.Journal of biochemical and molecular toxicology · 2026Review
- Prevalence and management practices of ophthalmic lesions in laboratory mice.Scientific reports · 2026Article
- Lens aging and disease: Molecular mechanisms, functional consequences, and pharmacological implications.Progress in retinal and eye research · 2026Review
- Non-canonical roles of Keap1/Nrf2 in regulating quiescence and early activation in adult muscle stem cells.Nature communications · 2025Article
- Pharmacological Strategies for Cataract Management: From Molecular Targets to Clinical Translation.International journal of molecular sciences · 2025Review
- Minimizing Oxidative Stress in the Lens: Alternative Measures for Elevating Glutathione in the Lens to Protect against Cataract.Antioxidants (Basel, Switzerland) · 2024Review
- Glycative stress as a cause of macular degeneration.Progress in retinal and eye research · 2024Review
- Oxidative stress in retinal pigment epithelium degeneration: from pathogenesis to therapeutic targets in dry age-related macular degeneration.Neural regeneration research · 2023Review
- Redox Regulation in Age-Related Cataracts: Roles for Glutathione, Vitamin C, and the NRF2 Signaling Pathway.Nutrients · 2023Review
- Hydralazine Revives Cellular and Ocular Lens Health-Span by Ameliorating the Aging and Oxidative-Dependent Loss of the Nrf2-Activated Cellular Stress Response.Antioxidants (Basel, Switzerland) · 2023Article
- Interplay between Nrf2 and αB-crystallin in the lens and heart of zebrafish under proteostatic stress.Frontiers in molecular biosciences · 2023Article
- Potential Properties of Natural Nutraceuticals and Antioxidants in Age-Related Eye Disorders.Life (Basel, Switzerland) · 2022Review
- Proteostasis in aging-associated ocular disease.Molecular aspects of medicine · 2022Review
- Dependence of Retinal Pigment Epithelium Integrity on the NRF2-Heme Oxygenase-1 Axis.Investigative ophthalmology & visual science · 2022Article
- Loss of fiber cell communication may contribute to the development of cataracts of many different etiologies.Frontiers in physiology · 2022Review
- Deficiency of the bZIP transcription factors Mafg and Mafk causes misexpression of genes in distinct pathways and results in lens embryonic developmental defects.Frontiers in cell and developmental biology · 2022Article
Corrections and comments
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Authors and funding
17 authors at 8 institutions in 1 country.
Funding
Abstract
Purpose: Age-related cataracts affect the majority of older adults and are a leading cause of blindness worldwide. Treatments that delay cataract onset or severity have the potential to delay cataract surgery, but require relevant animal models that recapitulate the major types of cataracts for their development. Unfortunately, few such models are available. Here, we report the lens phenotypes of aged mice lacking the critical antioxidant transcription factor Nfe2l2 (designated as Nrf2 -/-). Methods: Three independent cohorts of Nrf2 -/- and wild-type C57BL/6J mice were evaluated for cataracts using combinations of slit lamp imaging, photography of freshly dissected lenses, and histology. Mice were fed high glycemic diets, low glycemic diets, regular chow ad libitum, or regular chow with 30% caloric restriction. Results: Nrf2 -/- mice developed significant opacities between 11 and 15 months and developed advanced cortical, posterior subcapsular, anterior subcapsular, and nuclear cataracts. Cataracts occurred similarly in male mice fed high or low glycemic diets, and were also observed in 21-month male and female Nrf2 -/- mice fed ad libitum or 30% caloric restriction. Histological observation of 18-month cataractous lenses revealed significant disruption to fiber cell architecture and the retention of nuclei throughout the cortical region of the lens. However, fiber cell denucleation and initiation of lens differentiation was normal at birth, with the first abnormalities observed at 3 months. Conclusions: Nrf2 -/- mice offer a tool to understand how defective antioxidant signaling causes multiple forms of cataract and may be useful for screening drugs to prevent or delay cataractogenesis in susceptible adults.
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Registered trials
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