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Rowan S, Jiang S, Francisco SG, et al. Aged Nrf2-Null Mice Develop All Major Types of Age-Related Cataracts. Invest Ophthalmol Vis Sci. 2021;62(15):10doi: 10.1167/iovs.62.15.10.
Rowan, S., Jiang, S., Francisco, S. G., Pomatto, L. C. D., Ma, Z., Jiao, X., Campos, M. M., Aryal, S., Patel, S. D., Mahaling, B., Riazuddin, S. A., Duh, E. J., Lachke, S. A., Hejtmancik, J. F., de Cabo, R., FitzGerald, P. G., & Taylor, A. (2021). Aged Nrf2-Null Mice Develop All Major Types of Age-Related Cataracts. Investigative ophthalmology & visual science, 62(15), 10. https://doi.org/10.1167/iovs.62.15.10
Rowan, Sheldon, et al. "Aged Nrf2-Null Mice Develop All Major Types of Age-Related Cataracts." Investigative ophthalmology & visual science vol. 62,15 (2021): 10. doi: https://doi.org/10.1167/iovs.62.15.10
Rowan S, Jiang S, Francisco SG, Pomatto LCD, Ma Z, Jiao X, Campos MM, Aryal S, Patel SD, Mahaling B, Riazuddin SA, Duh EJ, Lachke SA, Hejtmancik JF, de Cabo R, FitzGerald PG, Taylor A. Aged Nrf2-Null Mice Develop All Major Types of Age-Related Cataracts. Invest Ophthalmol Vis Sci. 2021 Dec 01;62(15):10. doi: 10.1167/iovs.62.15.10. PMID: 34882206.
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Invest Ophthalmol Vis Sci. 2021 Dec 01;62(15):10. doi: 10.1167/iovs.62.15.10.

Aged Nrf2-Null Mice Develop All Major Types of Age-Related Cataracts.

Investigative ophthalmology & visual science

Sheldon Rowan, Shuhong Jiang, Sarah G Francisco, Laura C D Pomatto, Zhiwei Ma, Xiaodong Jiao, Maria M Campos, Sandeep Aryal, Shaili D Patel, Binapani Mahaling, S Amer Riazuddin, Elia J Duh, Salil A Lachke, J Fielding Hejtmancik, Rafael de Cabo, Paul G FitzGerald, Allen Taylor

Affiliations

  1. JM-USDA Human Nutrition Research Center on Aging, Tufts University, Boston, Massachusetts, United States.
  2. Department of Ophthalmology, Tufts University School of Medicine, Tufts University, Boston, Massachusetts, United States.
  3. Friedman School of Nutrition Science and Policy, Tufts University, Boston, Massachusetts, United States.
  4. Translational Gerontology Branch, National Institute on Aging, National Institute of Health, Baltimore, Maryland, United States.
  5. Ophthalmic Genetics and Visual Function Branch, National Eye Institute, National Institutes of Health, Bethesda, Maryland, United States.
  6. NEI Histology Core, National Eye Institute, National Institutes of Health, Bethesda, Maryland, United States.
  7. Department of Biological Sciences, University of Delaware, Newark, Delaware, United States.
  8. Department of Ophthalmology, The Wilmer Eye Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States.
  9. Center for Bioinformatics and Computational Biology, University of Delaware, Newark, Delaware, United States.
  10. Department of Cell Biology and Human Anatomy, School of Medicine, University of California Davis, Davis, California, United States.

PMID: 34882206 DOI: 10.1167/iovs.62.15.10

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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