ArticleThe Journal of cell biology1995
Lens epithelial cell apoptosis appears to be a common cellular basis for non-congenital cataract development in humans and animals.
Article in The Journal of cell biology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 132 papers.
What it found
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The trial behind it
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Who cites it
132 citing papers in PubMed, 400 citations in OpenAlex.
- Trial
- Lens aging and disease: Molecular mechanisms, functional consequences, and pharmacological implications.Progress in retinal and eye research · 2026Review
- Transcriptome RNA sequencing reveals the global molecular responses and circRNA-miRNA-lncRNA interaction network in cataract.Japanese journal of ophthalmology · 2026Article
- Aging of the human eye lens: Epigenetic landscape and therapeutic targets in age‑related cataracts (Review).International journal of molecular medicine · 2025Review
- Cellular Senescence in Health, Disease, and Lens Aging.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Protective effect of apelin-13 in lens epithelial cells via inhibiting oxidative stress-induced apoptosis.BMC ophthalmology · 2024Article
- Oxidative Stress in Cataract Formation: Is There a Treatment Approach on the Horizon?Antioxidants (Basel, Switzerland) · 2024Review
- Quantitative Factors Introduced in the Feasibility Analysis of Reactive Oxygen Species (ROS)-Sensitive Triggers.Angewandte Chemie (International ed. in English) · 2024Review
- Maf1 controls retinal neuron number by both RNA Pol III- and Pol II-dependent mechanisms.iScience · 2023Article
- SUMO1-regulated DBC1 promotes p53-dependent stress-induced apoptosis of lens epithelial cells.Aging · 2023Article
- Article
- HSP90β prevents aging-related cataract formation through regulation of the charged multivesicular body protein (CHMP4B) and p53.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- 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
- Investigation of the antioxidant effect of Chrysin in an experimental cataract model created in chick embryos.Molecular vision · 2023Article
- Article
- Diosmetin attenuates oxidative stress-induced damage to lens epithelial cells via the mitogen-activated protein kinase (MAPK) pathway.Bioengineered · 2022Article
- The E3 Ligase RNF157 Inhibits Lens Epithelial Cell Apoptosis by Negatively Regulating p53 in Age-Related Cataracts.Investigative ophthalmology & visual science · 2022Article
- Thiol antioxidants protect human lens epithelial (HLE B-3) cells againstBiochemistry and biophysics reports · 2022Article
- Autophagy facilitates age-related cell apoptosis-a new insight from senile cataract.Cell death & disease · 2022Article
- Differentially expressed gene profiles and associated ceRNA network in ATG7-Deficient lens epithelial cells under oxidative stress.Frontiers in genetics · 2022Article
72 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Cataract is a major ocular disease that causes blindness in many developing countries of the world. It is well established that various factors such as oxidative stress, UV, and other toxic agents can induce both in vivo and in vitro cataract formation. However, a common cellular basis for this induction has not been previously recognized. The present study of lens epithelial cell viability suggests such a general mechanism. When lens epithelial cells from a group of 20 cataract patients 12 to 94 years old were analyzed by terminal deoxynucleotidyl transferase (TdT) labeling and DNA fragmentation assays, it was found that all of these patients had apoptotic epithelial cells ranging from 4.4 to 41.8%. By contrast, in eight normal human lenses of comparable age, very few apoptotic epithelial cells were observed. We suggest that cataract patients may have deficient defense systems against factors such as oxidative stress and UV at the onset of the disease. Such stress can trigger lens epithelial cell apoptosis that then may initiate cataract development. To test this hypothesis, it is also demonstrated here that hydrogen peroxide at concentrations previously found in some cataract patients induces both lens epithelial cell apoptosis and cortical opacity. Moreover, the temporal and spatial distribution of induced apoptotic lens epithelial cells precedes development of lens opacification. These results suggest that lens epithelial cell apoptosis may be a common cellular basis for initiation of noncongenital cataract formation.
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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.