Evidence map›Paper›PMID 35408826›Full record

ArticleInternational journal of molecular sciences2022

Role of ERK Pathway in the Pathogenesis of Atopic Dermatitis and Its Potential as a Therapeutic Target.

Nahoko Zeze, Makiko Kido-Nakahara, Gaku Tsuji, Eriko Maehara, Yuki Sato, Sawako Sakai, Kei Fujishima, Akiko Hashimoto-Hachiya, Masutaka Furue, Takeshi Nakahara

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
6.1field-weighted citation impact, top 3% of its field
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

24 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
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  6. The Anti-Inflammatory and Skin Barrier Function Recovery Effects ofInternational journal of molecular sciences · 2025
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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

10 authors at 1 institution in 1 country.

Nahoko ZezeDepartment of Dermatology, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan.
Makiko Kido-NakaharaDepartment of Dermatology, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan.
Gaku TsujiDepartment of Dermatology, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan.
Eriko MaeharaDepartment of Dermatology, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan.
Yuki SatoDepartment of Dermatology, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan.
Sawako SakaiDepartment of Dermatology, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan.
Kei FujishimaDepartment of Dermatology, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan.
Akiko Hashimoto-HachiyaDepartment of Dermatology, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan.
Masutaka FurueDepartment of Dermatology, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan.ORCID 0000-0002-2967-1073
Takeshi NakaharaDepartment of Dermatology, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan.
Kyushu University · JP

Funding

Japan Society for the Promotion of Science 21K08350
6 · The paper itself

Abstract

Atopic dermatitis (AD) is an eczematous skin disorder characterized by type 2 inflammation, barrier disruption, and intense itch. In addition to type 2 cytokines, many other cytokines, such as interferon gamma (IFN-γ), interleukin 17 (IL-17), and interleukin 22 (IL-22), play roles in the pathogenesis of AD. It has been reported that the extracellular signal-regulated kinase (ERK) is downstream of such cytokines. However, the involvement of the ERK pathway in the pathogenesis of AD has not yet been investigated. We examined the expression of p-ERK in mouse and human AD skin. We also investigated the effects of the topical application of an ERK inhibitor on the dermatitis score, transepidermal water loss (TEWL), histological change, and expression of filaggrin, using an AD-like NC/Nga murine model. The effects of an ERK inhibitor on filaggrin expression in normal human epidermal keratinocytes (NHEKs) and on chemokine production from bone marrow-derived dendritic cells (BMDCs) were also evaluated. p-ERK was highly expressed in mouse and human AD skin. Topical application of an ERK inhibitor alleviated the clinical symptoms, histological changes, TEWL, and decrease in expression of filaggrin in the AD-like NC/Nga murine model. The ERK inhibitor also restored the IL-4 induced reduction in the expression of filaggrin in NHEK, and inhibited chemokine production from BMDC induced by IL-4. These results indicate that the ERK pathway is involved in the pathogenesis of AD, and suggest that the ERK pathway has potential as a therapeutic target for AD in the future.

Indexed as

Dermatitis, AtopicAnimalsChemokinesCytokinesDisease Models, AnimalExtracellular Signal-Regulated MAP KinasesInterleukin-4MAP Kinase Signaling SystemMiceSkinChemokinesCytokinesExtracellular Signal-Regulated MAP KinasesInterleukin-4atopic dermatitisbarrier functionERK pathwayfilaggrinTEWL

Identifiers

PMID35408826
PMCPMC8999015
OpenAlexW4220989258

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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.