Evidence map›Paper›PMID 39744884›Full record

ArticleDisease models & mechanisms2025

Dose-dependent effects of Nrf2 on the epidermis in chronic skin inflammation.

Michael Koch, Luca Ferrarese, Maya Ben-Yehuda Greenwald, Sabine Werner

Abstract read
In one paragraph

Article in Disease models & mechanisms, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed.

  1. Review
  2. Review
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  5. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Michael KochInstitute of Molecular Health Sciences, Department of Biology, ETH Zürich, 8093 Zürich, Switzerland.ORCID 0000-0003-2797-3227
Luca FerrareseInstitute of Molecular Health Sciences, Department of Biology, ETH Zürich, 8093 Zürich, Switzerland.
Maya Ben-Yehuda GreenwaldInstitute of Molecular Health Sciences, Department of Biology, ETH Zürich, 8093 Zürich, Switzerland.ORCID 0000-0002-6089-0856
Sabine WernerInstitute of Molecular Health Sciences, Department of Biology, ETH Zürich, 8093 Zürich, Switzerland.ORCID 0000-0001-7397-8710

Funding

Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung 310030-212212
6 · The paper itself

Abstract

Atopic dermatitis (AD) is a chronic inflammatory skin disease, characterized by an impaired epidermal barrier and immunological alterations. The activity of the cytoprotective NRF2 transcription factor is reduced in the epidermis of AD patients. To determine the functional relevance of this deficiency, we used mice lacking fibroblast growth factor receptors 1 and 2 in keratinocytes (K5-R1/R2 mice), which exhibit several AD-like symptoms. Proteomics analysis of their epidermis revealed reduced Nrf2 activity. This was accompanied by an increase in DNA damage and in the number of senescent cells. Genetic deletion of Nrf2 in keratinocytes of these mice further promoted DNA damage and senescence, but time-limited pharmacological activation of Nrf2 in the skin had a mild protective effect. Surprisingly, long-term genetic activation of Nrf2 in keratinocytes of K5-R1/R2 mice caused strong hyperkeratosis, keratinocyte hyperproliferation, epidermal thickening, increased keratinocyte apoptosis and DNA damage, and altered immune cell composition. These results reveal a complex role of Nrf2 in the epidermis and show the necessity to optimize the duration and intensity of NRF2 activation for the treatment of epidermal alterations in patients with AD.

Indexed as

DNA DamageEpidermisInflammationKeratinocytesNF-E2-Related Factor 2AnimalsApoptosisCell ProliferationCellular SenescenceChronic DiseaseDermatitis, AtopicMiceMice, Inbred C57BLNfe2l2 protein, mouseNF-E2-Related Factor 2Atopic dermatitisCytoprotectionFGFKeratinocyteNrf2Skin

Identifiers

PMID39744884
PMCPMC11708820

What Socratic holds

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Registered trials

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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 Socratic graph.