ArticleProceedings of the National Academy of Sciences of the United States of America2020
Ultraviolet A light induces DNA damage and estrogen-DNA adducts in Fuchs endothelial corneal dystrophy causing females to be more affected.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.
What it found
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The trial behind it
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Who cites it
88 citing papers in PubMed, 144 citations in OpenAlex.
- Sex-Specific Differences in Corneal Remodeling after Descemet Membrane Endothelial Keratoplasty in Fuchs Endothelial Corneal Dystrophy.Ophthalmology science · 2026Article
- A Viscous DES-AAV-Foxo1 Delivery System With High Transfection Efficiency for the Treatment of Corneal Endothelial Dysfunction by Restoring Mitochondria-ER Contacts.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- NAMPT Deficiency Promotes Endothelial-Mesenchymal Transition by Inhibiting Energy Metabolism and Lysosomal Acidification in Late-Onset Fuchs Endothelial Corneal Dystrophy.Investigative ophthalmology & visual science · 2026Article
- PEDF Prevents Corneal Endothelial Dysfunction of Fuchs Endothelial Corneal Dystrophy.Investigative ophthalmology & visual science · 2026Article
- Exploring the histopathological signature of repeat-mediated Fuchs endothelial corneal dystrophy.Acta ophthalmologica · 2026Article
- Sex differences in congenital hereditary endothelial dystrophy (CHED) and Slc4a11Biology of sex differences · 2026Article
- TAZ (bioRxiv : the preprint server for biology · 2026Article
- Taurochenodeoxycholic Acid Activates Calcium Signaling to Protect Against Fuchs' Endothelial Corneal Dystrophy.Investigative ophthalmology & visual science · 2026Article
- p16-mediated G0/G1 cell cycle arrest leads to SASP and fibrosis in Fuchs endothelial corneal dystrophy.Cell death & disease · 2026Article
- ATF4 regulates mitochondrial dysfunction and mitophagy, contributing to corneal endothelial apoptosis.Scientific reports · 2026Article
- Fuchs Endothelial Corneal Dystrophy Associations with Systemic Disease, Lifestyle, and Nutritional Intake.Ophthalmology science · 2026Article
- A novel single-cell level evaluation method for corneal endothelial cell function.NPJ digital medicine · 2025Article
- Blockade of mitochondrial components release by exosome pathway promotes the pathogenesis of Fuchs endothelial corneal dystrophy.Cell death discovery · 2025Article
- Protective Effects of Estradiol on Disease Progression in a Murine Model of Fuchs Endothelial Corneal Dystrophy.Investigative ophthalmology & visual science · 2025Article
- Transcriptome analyses of human corneal endothelial cell lines derived from patients with Fuchs endothelial corneal dystrophy.Scientific reports · 2025Article
- Permanent Senescence Via p16 Leads to Guttae Formation in an In Vitro Human Corneal Endothelial Cell Model.Investigative ophthalmology & visual science · 2025Article
- A bioequivalent cornea cross-linking method using photo-initiators LAP and visible light.Materials today. Bio · 2025Article
- Morphological Features in Eyes with Prominent Corneal Endothelial Cell Loss Associated with Primary Angle-Closure Disease.Journal of clinical medicine · 2025Article
- Current and Future Cornea Chip Models for Advancing Ophthalmic Research and Therapeutics.Advanced biology · 2025Review
- Generation of a Mouse Model of Fuchs Endothelial Corneal Dystrophy by Knock-in of CTG Trinucleotide Repeat Expansion in the TCF4 Gene.Investigative ophthalmology & visual science · 2025Article
28 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 1 country.
Funding
Abstract
Fuchs endothelial corneal dystrophy (FECD) is a leading cause of corneal endothelial (CE) degeneration resulting in impaired visual acuity. It is a genetically complex and age-related disorder, with higher incidence in females. In this study, we established a nongenetic FECD animal model based on the physiologic outcome of CE susceptibility to oxidative stress by demonstrating that corneal exposure to ultraviolet A (UVA) recapitulates the morphological and molecular changes of FECD. Targeted irradiation of mouse corneas with UVA induced reactive oxygen species (ROS) production in the aqueous humor, and caused greater CE cell loss, including loss of ZO-1 junctional contacts and corneal edema, in female than male mice, characteristic of late-onset FECD. UVA irradiation caused greater mitochondrial DNA (mtDNA) and nuclear DNA (nDNA) damage in female mice, indicative of the sex-driven differential response of the CE to UVA, thus accounting for more severe phenotype in females. The sex-dependent effect of UVA was driven by the activation of estrogen-metabolizing enzyme CYP1B1 and formation of reactive estrogen metabolites and estrogen-DNA adducts in female but not male mice. Supplementation of
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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.