ArticleChemico-biological interactions2012
Age-related cataracts: homocysteine coupled endoplasmic reticulum stress and suppression of Nrf2-dependent antioxidant protection.
Article in Chemico-biological interactions, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
38 citing papers in PubMed, 64 citations in OpenAlex.
- DNA hypermethylation-mediated downregulation of antioxidant genes contributes to the early onset of cataracts in highly myopic eyes.Redox biology · 2018Trial
- Review
- Aging, oxidative stress, and cataracts: Therapeutic prospects and translational insights into peroxiredoxin 6.Progress in retinal and eye research · 2026Review
- Lens aging and disease: Molecular mechanisms, functional consequences, and pharmacological implications.Progress in retinal and eye research · 2026Review
- Frailty-Driven Risk Stratification in Age-Related Ophthalmic Diseases: Thresholds, Precision Screening, and Mendelian Randomization Insights.Translational vision science & technology · 2025Article
- TRB3 Promotes Cataract Progression through Endoplasmic Reticulum Stress-mediated Mitochondrial Dysfunction and Cell Apoptosis.Cell biochemistry and biophysics · 2025Article
- Associations of severe liver diseases with cataract using data from UK Biobank: a prospective cohort study.EClinicalMedicine · 2024Article
- Antioxidant System and Endoplasmic Reticulum Stress in Cataracts.Cellular and molecular neurobiology · 2023Review
- Redox Regulation in Age-Related Cataracts: Roles for Glutathione, Vitamin C, and the NRF2 Signaling Pathway.Nutrients · 2023Review
- Alu antisense RNA ameliorates methylglyoxal-induced human lens epithelial cell apoptosis by enhancing antioxidant defense.International journal of ophthalmology · 2023Article
- Protective effects of ferulic acid against ionizing radiation-induced oxidative damage in rat lens through activating Nrf2 signal pathway.International journal of ophthalmology · 2023Article
- Senescence marker protein30 protects lens epithelial cells against oxidative damage by restoring mitochondrial function.Bioengineered · 2022Article
- Aged Nrf2-Null Mice Develop All Major Types of Age-Related Cataracts.Investigative ophthalmology & visual science · 2021Article
- Nuclear Factor Erythroid-2-Related Factor 2 Signaling in the Neuropathophysiology of Inherited Metabolic Disorders.Frontiers in cellular neuroscience · 2021Review
- Gastrodin prevents homocysteine-induced human umbilical vein endothelial cells injury via PI3K/Akt/eNOS and Nrf2/ARE pathway.Journal of cellular and molecular medicine · 2021Article
- The Protective Effects of Flavonoids in Cataract Formation through the Activation of Nrf2 and the Inhibition of MMP-9.Nutrients · 2020Review
- Diabetic Retinopathy: Mitochondria Caught in a Muddle of Homocysteine.Journal of clinical medicine · 2020Review
- Redox toxicology of environmental chemicals causing oxidative stress.Redox biology · 2020Review
- p62/Sequestosome 1 levels increase and phosphorylation is altered in Cx50D47A lenses, but deletion of p62/sequestosome 1 does not improve transparency.Molecular vision · 2020Article
- Polyphenol-enriched fraction ofMolecular vision · 2019Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
To determine whether high levels of homocysteine (Hcy) induce endoplasmic reticulum (ER) stress with suppression of the nuclear factor-erythroid-2-related factor 2 (Nrf2)-dependent antioxidant protection in lens epithelial cells (LECs). ER stress was acutely induced by exposure of LECs to 100 μM Hcy without FCS and also by exposure to 5 mM Hcy with 10% FCS. After exposure to Hcy, significant changes were found in P-PERK, P-eIF2α, XBP1, Nrf2, and Keap1 within 24 h. The production of reactive oxygen species (ROS) was increased after Hcy exposure. The downstream enzymes of Nrf2 like, catalase, and glutathione reductase, were significantly decreased. These results suggested that the Hcy-induced ER stress suppressed the Nrf2-dependent antioxidant protection and simultaneously generated ROS which resulted in further oxidation and death of LECs. The loss of Nrf2 is mainly due to proteosomal degradation and m-calpain activation by the increased levels of cytoplasmic Ca(++). The caspases also play a role in the degradation of Nrf2. Our findings demonstrated that high levels of Hcy induce ER stress, chronic UPR, alter the levels of UPR specific proteins, increase the production of ROS, degrade Nrf2 and block the Nrf2-dependent antioxidant defense protection in LECs. Thus, the upregulation of ROS might exceed the Nrf2 dependent antioxidant defense protection in the LECs and result in the highly oxidized lenses and resulted in ARCs.
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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.