ArticleCommunications biology2024
Modulation of ATM enhances DNA repair in G2/M phase of cell cycle and averts senescence in Fuchs endothelial corneal dystrophy.
Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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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
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Who cites it
13 citing papers in PubMed.
- LSD1-mediated demethylation of the DNA damage response factor ATM promotes senescence and organ aging.The Journal of clinical investigation · 2026Article
- An integrated multi-algorithm analysis to decipher senescence and metabolic characteristics in nucleus pulposus cells during disc degeneration.GeroScience · 2026Article
- GATA4-Driven Transcription of HtrA1 Promotes Cellular Senescence in Ménière's Disease and Age-Related Audio-Vestibular Dysfunction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The cGAS-STING pathway in senescence and aging-related diseases: mechanisms and therapeutic opportunities.Cell communication and signaling : CCS · 2026Review
- Cancer and aging: complex associations and therapeutic targets.Molecular biomedicine · 2026Review
- Differential regulation of radioadaptation by quercetin between human normal and cancer cells.Clinical and translational radiation oncology · 2026Article
- p16-mediated G0/G1 cell cycle arrest leads to SASP and fibrosis in Fuchs endothelial corneal dystrophy.Cell death & disease · 2026Article
- 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
- DNA Damage Response Regulation Alleviates Neuroinflammation in a Mouse Model of α-Synucleinopathy.Biomolecules · 2025Article
- ATM and p53 in aging and cancer: a double-edged sword in genomic integrity.Biogerontology · 2025Review
- Up-regulated microRNAs in blastocoel fluid of human implanted embryos could control circuits of pluripotency and be related to embryo competence.Journal of assisted reproduction and genetics · 2025Article
- Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Fuchs Endothelial Corneal Dystrophy (FECD) is an aging disorder characterized by expedited loss of corneal endothelial cells (CEnCs) and heightened DNA damage compared to normal CEnCs. We previously established that ultraviolet-A (UVA) light causes DNA damage and leads to FECD phenotype in a non-genetic mouse model. Here, we demonstrate that acute treatment with chemical stressor, menadione, or physiological stressors, UVA, and catechol estrogen (4-OHE
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Registered trials
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