ArticleScientific reports2025
Topical application of the HSP90 inhibitor 17-AAG reduces skin inflammation and partially restores microbial balance: implications for atopic dermatitis therapy.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- Hsp90 as a pathophysiological factor and emerging therapeutic target in atopic dermatitis.Frontiers in immunology · 2025Review
Corrections and comments
- Erratum issued
Authors and funding
7 authors.
Funding
Abstract
Heat shock proteins belonging to the HSP90 family promote inflammation and are potential therapeutic targets in inflammatory and autoimmune diseases. Here the effects of the HSP90 inhibitor 17-AAG applied topically were evaluated in a DNCB-induced murine model of atopic dermatitis (AD). The use of 17-AAG improved clinical disease activity without causing toxicity in the animals. Topical application of 17-AAG resulted in reduced epidermal hyperplasia, decreased expression of TSLP, IL-5, and IL-6, as well as reduced activation of NF-κB in the skin. In addition, the eosinophil proportion in the blood and eosinophil peroxidase (EPX) activity in the skin were significantly reduced in 17-AAG-treated AD mice. The inhibitory effects of 17-AAG on the production of epidermal alarmins, T-helper cell-associated cytokines, and ROS release were demonstrated in cultures of activated human keratinocytes, CD4
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