ArticleThe Journal of biological chemistry2014
Glutaredoxin 2 (Grx2) gene deletion induces early onset of age-dependent cataracts in mice.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 56 citations in OpenAlex.
- Hydrogen peroxide sensing and signaling in physiology and disease: implications for therapy.Signal transduction and targeted therapy · 2026Review
- Grx2 deficiency accelerates BMSC senescence and senile osteoporosis via CD36 S-glutathionylation.Cellular & molecular biology letters · 2026Article
- Fullerenol Eye Drops Mitigate UVB-Induced Cataract Progression by Inhibiting Oxidative Stress and Cellular Senescence.Antioxidants (Basel, Switzerland) · 2026Article
- Glutaredoxin 2 Protects Lens Epithelial Cells From Ferroptosis by Preventing HNRNPA2B1 S-Glutathionylation in Diabetes-Mediated Cataractogenesis.Investigative ophthalmology & visual science · 2025Article
- A Reassessment of Sarcopenia from a Redox Perspective as a Basis for Preventive and Therapeutic Interventions.International journal of molecular sciences · 2025Review
- Glutaredoxin2 reduces age-associated B cell differentiation through maintaining redox homeostasis.Frontiers in pharmacology · 2025Article
- A grape-supplemented diet prevented ultraviolet (UV) radiation-induced cataract by regulating Nrf2 and XIAP pathways.The Journal of nutritional biochemistry · 2024Article
- Antioxidant System and Endoplasmic Reticulum Stress in Cataracts.Cellular and molecular neurobiology · 2023Review
- A tamoxifen-inducible Cre knock-in mouse for lens-specific gene manipulation.Experimental eye research · 2023Article
- Regulation of Mitochondrial Hydrogen Peroxide Availability by Protein S-glutathionylation.Cells · 2022Review
- Conditions Conducive to the Glutathionylation of Complex I Subunit NDUFS1 Augment ROS Production following the Oxidation of Ubiquinone Linked Substrates, Glycerol-3-Phosphate and Proline.Antioxidants (Basel, Switzerland) · 2022Article
- S-Denitrosylation: A Crosstalk between Glutathione and Redoxin Systems.Antioxidants (Basel, Switzerland) · 2022Review
- Trabecular Meshwork Mitochondrial Function and Oxidative Stress: Clues to Racial Disparities of Glaucoma.Ophthalmology science · 2022Article
- A macrocyclic molecule with multiple antioxidative activities protects the lens from oxidative damage.Frontiers in chemistry · 2022Article
- Aged Nrf2-Null Mice Develop All Major Types of Age-Related Cataracts.Investigative ophthalmology & visual science · 2021Article
- An investigation into the impact of deleting one copy of theRedox report : communications in free radical research · 2020Article
- S-glutathionylation, friend or foe in cardiovascular health and disease.Redox biology · 2020Review
- Protein S-glutathionylation reactions as a global inhibitor of cell metabolism for the desensitization of hydrogen peroxide signals.Redox biology · 2020Review
- Modulation of Reactive Oxygen Species in Health and Disease.Antioxidants (Basel, Switzerland) · 2019Article
- Sex-dependent Differences in the Bioenergetics of Liver and Muscle Mitochondria from Mice Containing a Deletion forAntioxidants (Basel, Switzerland) · 2019Article
Corrections and comments
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Authors and funding
5 authors at 5 institutions in 2 countries.
Funding
Abstract
Glutaredoxin 2 (Grx2) is an isozyme of glutaredoxin1 (thioltransferase) present in the mitochondria and nucleus with disulfide reductase and peroxidase activities, and it controls thiol/disulfide balance in cells. In this study, we investigated whether Grx2 gene deletion could induce faster age-related cataract formation and elucidated the biochemical changes effected by Grx2 gene deletion that may contribute to lens opacity. Slit lamp was used to examine the lenses in Grx2 knock-out (KO) mice and age-matched wild-type (WT) mice ages 1 to 16 months. In the Grx2 null mice, the lens nuclear opacity began at 5 months, 3 months sooner than that of the control mice, and the progression of cataracts was also much faster than the age-matched controls. Lenses of KO mice contained lower levels of protein thiols and GSH with a significant accumulation of S-glutathionylated proteins. Actin, αA-crystallin, and βB2-crystallin were identified by Western blot and mass spectroscopy as the major S-glutathionylated proteins in the lenses of 16-month-old Grx2 KO mice. Compared with the WT control, the lens of Grx2 KO mice had only 50% of the activity in complex I and complex IV and less than 10% of the ATP pool. It was concluded that Grx2 gene deletion altered the function of lens structural proteins through S-glutathionylation and also caused severe disturbance in mitochondrial function. These combined alterations affected lens transparency.
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Registered trials
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