ArticleClinical, cosmetic and investigational dermatology2025
Ellagic Acid Mediates the Delay of Dermal Fibroblast Senescence via CSNK2A1.
Article in Clinical, cosmetic and investigational dermatology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Integrated Transcriptomics and Experimental Validation Reveal That Ellagic Acid Alleviates Fuchs Endothelial Corneal Dystrophy via PLAU/NF-κB Signaling.Investigative ophthalmology & visual science · 2026Article
- An Insight on Ellagic Acid Formulations for the Management of Skin Diseases.Molecules (Basel, Switzerland) · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: This research seeks to explore the impact of Ellagic Acid (EA) on the aging process of human dermal fibroblasts Hs68 cells and to uncover the mechanisms involved. Methods: Senescence was induced in Hs68 cells with H Results: Senescent cells showed increased γH2AX, p16, p19, and p53 expression, with reduced viability. EA inhibited senescence in a dose-dependent manner, with cytotoxicity at 60 μM. EA upregulated CSNK2A1, decreased β-galactosidase activity, restored cell viability and cycle progression, and reduced apoptosis. EA alleviated oxidative stress by enhancing Nrf2 expression, reducing ROS and MDA, and increasing SOD and GSH/GSSG. Silmitasertib negated these effects. EA also reduced IL-6, TNF-α, and IL-1β, inhibiting NF-κB p65, with anti-inflammatory effects mediated by CSNK2A1. Conclusion: EA delays dermal fibroblast senescence by modulating CSNK2A1, mitigating oxidative stress and inflammation, and may serve as a potential therapeutic for aging and age-related diseases.
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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.