Evidence map›Paper›PMID 39207509›Full record

ArticleArchives of dermatological research2024

Benvitimod upregulates filaggrin, involucrin and loricrin expressions via aryl hydrocarbon receptor-OVO-like 1 axis.

Qiuyu Jia, Ping Liu, Xiaojie Wang, Jian Hu, Jun Jia, Jianzhong Zhang, Houmin Li

Abstract read
In one paragraph

Article in Archives of dermatological research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Role of the STAT3 Signaling Pathway in Cell Proliferation and Inflammation in Psoriasis and Approaches for Targeted Therapies: A Review.Medical science monitor : international medical journal of experimental and clinical research · 2026
    Review
  4. 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

7 authors.

Qiuyu Jia *Department of Dermatology, Peking University People's Hospital, No.11 Xizhimen South Street, Xicheng District, Beijing, 100044, China.ORCID http://orcid.org/0000-0001-9515-8203
Ping Liu *Department of Dermatology, Peking University People's Hospital, No.11 Xizhimen South Street, Xicheng District, Beijing, 100044, China.ORCID http://orcid.org/0009-0002-6102-5028
Xiaojie WangDepartment of Dermatology, Peking University People's Hospital, No.11 Xizhimen South Street, Xicheng District, Beijing, 100044, China.ORCID http://orcid.org/0000-0002-2616-3196
Jian HuDepartment of Dermatology, Peking University People's Hospital, No.11 Xizhimen South Street, Xicheng District, Beijing, 100044, China.ORCID http://orcid.org/0000-0002-1847-1404
Jun JiaDepartment of Dermatology, Peking University People's Hospital, No.11 Xizhimen South Street, Xicheng District, Beijing, 100044, China.ORCID http://orcid.org/0000-0001-9321-1226
Jianzhong ZhangDepartment of Dermatology, Peking University People's Hospital, No.11 Xizhimen South Street, Xicheng District, Beijing, 100044, China. rmzjz@126.com.ORCID http://orcid.org/0000-0002-5485-682X
Houmin LiDepartment of Dermatology, Peking University People's Hospital, No.11 Xizhimen South Street, Xicheng District, Beijing, 100044, China. lhoumin@sina.cn.ORCID http://orcid.org/0000-0002-1446-3466

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Benvitimod has been successfully used in the treatment of psoriasis and atopic dermatitis (AD). However, the mechanism remains to be clarified. We aim to assess the effects of benvitimod on MC903-induced dermatitis in mice and to investigate the effects of benvitimod on filaggrin (FLG), involucrin (IVL), and loricrin (LOR) expressions and possible mechanism. MC903-induced mouse AD model was used to evaluate the effects of benvitimod. Filaggrin, involucrin, and loricrin protein and mRNA expressions in lesions of mice dermatitis were measured by Western blot and quantitative real-time PCR. In vitro, normal human epidermal keratinocytes (NHEKs) were cultured and benvitimod was used to treat NHEKs primed with IL-4 and IL-13. Then AHR and OVOL1 in NHEKs were knocked down to evaluate the role of AHR and OVOL1 in the effects of benvitimod. Topical treatment of benvitimod repaired skin barrier and alleviated skin inflammation in mouse AD model. This effect was inhibited by pretreatment with an AHR antagonist. Benvitimod upregulated the filaggrin, involucrin, and loricrin expressions in lesions of mouse AD model. In addition, benvitimod upregulated the filaggrin, involucrin, and loricrin expressions in NHEKs. Knockdown of AHR or OVO-like (OVOL)1 abrogated the upregulation of filaggrin, involucrin, and loricrin induced by benvitimod. Benvitimod attenuated MC903-induced mouse dermatitis and upregulated filaggrin, involucrin, and loricrin expressions via AHR-OVOL1 axis.

Indexed as

Dermatitis, AtopicDisease Models, AnimalFilaggrin ProteinsIntermediate Filament ProteinsKeratinocytesProtein PrecursorsReceptors, Aryl HydrocarbonUp-RegulationAnimalsCells, CulturedDNA-Binding ProteinsHumansMembrane ProteinsMiceMice, Inbred BALB CSignal TransductionDNA-Binding ProteinsFilaggrin ProteinsFLG protein, humanIntermediate Filament ProteinsinvolucrinloricrinMembrane ProteinsOVOL1 protein, humanProtein PrecursorsReceptors, Aryl HydrocarbonTranscription FactorsAryl hydrocarbon receptorBenvitimodFilaggrinInvolucrin and OVOL1Loricrin

Identifiers

PMID39207509
PMCPMC11362246

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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 OpenQuestion graph.