ArticleThe Journal of dermatology2018
Fluorofenidone inhibits UV-A induced senescence in human dermal fibroblasts via the mammalian target of rapamycin-dependent SIRT1 pathway.
Article in The Journal of dermatology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
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.
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Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.
- Pooled it
- Longevity-Associated Transcription Factor ATF7 Promotes Healthspan by Suppressing Cellular Senescence and Systematic Inflammation.Aging and disease · 2023Article
- The role of sirtuins in dermal fibroblast function.Frontiers in medicine · 2023Review
- Shedding Light on the Effects of Calorie Restriction and its Mimetics on Skin Biology.Nutrients · 2020Review
- Purified Vitexin Compound 1 Inhibits UVA-Induced Cellular Senescence in Human Dermal Fibroblasts by Binding Mitogen-Activated Protein Kinase 1.Frontiers in cell and developmental biology · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of this study was to investigate the protective effect of fluorofenidone (5-methyl-1-[3-fluorophenyl]-2-[1H]-pyridone, AKF-PD) on ultraviolet (UV)-A-induced senescence in human dermal fibroblasts (HDF) and examine the mechanisms involved. HDF were treated with AKF-PD. Senescence-associated (SA)-β-galactosidase level, cell viability and expression of p16 were evaluated. In addition, UV-A-irradiated HDF were treated with AKF-PD, rapamycin and MHY1485; SA-β-galactosidase staining, 3-(4 5-dimethylthiazol-2-yl)-2 5-diphenyltetrazolium bromide assay and western blot for SIRT1 were performed; and phosphorylated mammalian target of rapamycin (p-mTOR) expression and reactive oxygen species (ROS) levels were measured. Intracellular ROS was detected by the 2',7'-dichlorofluroescein diacetate probe. Our results showed that AKF-PD substantially attenuated the changes of p16 expression, SA-β-galactosidase staining and cellular proliferation induced by UV-A irradiation in HDF. AKF-PD rescued the increased mTOR phosphorylation and reduced SIRT1 expression induced by UV-A irradiation in HDF. AKF-PD and rapamycin together had a synergistic effect on p-mTOR reduction and SIRT1 increase. mTOR activator MHY1485 partly blocked the above effects. Moreover, intracellular ROS level induced by UV-A irradiation could partly decrease by AKF-PD, and MHY1485 could reduce this effect. Our results indicated that AKF-PD could alleviate HDF senescence induced by UV-A-irradiation by inhibiting the p-mTOR and increasing SIRT1. Moreover, AKF-PD may be a potential treatment material for skin.
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