ArticleExperimental dermatology2020
Voriconazole enhances UV-induced DNA damage by inhibiting catalase and promoting oxidative stress.
Article in Experimental dermatology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- Integration of FAERS database and network toxicology to investigate adverse drug events and potential toxicological mechanisms of triazole antifungal agents.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Pharmacogenetics of steady-state metabolism, pharmacokinetics, and adverse effects of voriconazole in healthy participants.Drug metabolism and disposition: the biological fate of chemicals · 2025Article
- Pulmonary arterial hypertension caused by coadministration of dasatinib and voriconazole: A case report and literature review.Medicine · 2025Review
- Effect of Combination of Blue and Red Light with Terbinafine on Cell Viability and Reactive Oxygen Species in Human Keratinocytes: Potential Implications for Cutaneous Mycosis.International journal of molecular sciences · 2024Article
- Sustained Release of Voriconazole Using 3D-Crosslinked Hydrogel Rings and Rods for Use in Corneal Drug Delivery.Gels (Basel, Switzerland) · 2023Article
- Drug Discovery Targeting Post-Translational Modifications in Response to DNA Damages Induced by Space Radiation.International journal of molecular sciences · 2023Review
- Review
- Cutaneous Squamous Cell Carcinoma: From Biology to Therapy.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
22 authors at 2 institutions in 1 country.
Funding
Abstract
Cutaneous squamous cell carcinoma (cSCC) is the second most common form of skin cancer and is associated with cumulative UV exposure. Studies have shown that prolonged voriconazole use promotes cSCC formation; however, the biological mechanisms responsible for the increased incidence remain unclear. Here, we show that voriconazole directly increases oxidative stress in human keratinocytes and promotes UV-induced DNA damage as determined by comet assay, 8-oxoguanine immunofluorescence and mass spectrometry. Voriconazole treatment of human keratinocytes potentiates UV-induced apoptosis and activation of the p38 MAP kinase and 53BP1 UV stress response pathways. The p38 MAP kinase activation promoted by voriconazole exposure can be mitigated by pretreating keratinocytes with N-acetylcysteine. Voriconazole increases oxidative stress in keratinocytes by directly inhibiting catalase leading to lower intracellular NADPH levels and the triazole moieties in voriconazole are critical for inhibiting catalase. Furthermore, voriconazole is shown to promote UV-induced dysplasia in an in vivo model. Together, these data demonstrate that voriconazole potentiates oxidative stress in UV-irradiated keratinocytes through catalase inhibition. Use of antioxidants may mitigate the pro-oncogenic effects of voriconazole.
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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.