Evidence map›Paper›PMID 29259713›Full record

ReviewInflammation and regeneration2017

The etiopathogenesis of atopic dermatitis: barrier disruption, immunological derangement, and pruritus.

Pawinee Rerknimitr, Atsushi Otsuka, Chisa Nakashima, Kenji Kabashima

Open access · goldAbstract readReview
In one paragraph

Review in Inflammation and regeneration, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed, 2 pooled it
15.1field-weighted citation impact, top 1% 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

79 citing papers in PubMed, 2 syntheses or guidelines pooled it, 186 citations in OpenAlex.

  1. Pooled it
  2. Interventions for pityriasis rosea.The Cochrane database of systematic reviews · 2019
    Pooled it
  3. Trial
  4. Trial
  5. Identification of two early life eczema and non-eczema phenotypes with high risk for asthma development.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2019
    Trial
  6. Article
  7. Ameliorative effects ofMolecular medicine reports · 2026
    Article
  8. Review
  9. Article
  10. AAntioxidants (Basel, Switzerland) · 2026
    Article
  11. Review
  12. Targeting the TOPK-STAT3 pathway in keratinocytes and mast cells mediates the therapeutic attenuation of Atopic dermatitis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Pathogens (Basel, Switzerland) · 2025
    Article
  18. Review
  19. Article
  20. Article

19 more citing papers are in PubMed but not listed here.

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 at 1 institution in 2 countries.

Pawinee RerknimitrDepartment of Dermatology, Kyoto University Graduate School of Medicine, 54 Shogoin-Kawara, Sakyo, Kyoto, 606-8507 Japan.
Atsushi OtsukaDepartment of Dermatology, Kyoto University Graduate School of Medicine, 54 Shogoin-Kawara, Sakyo, Kyoto, 606-8507 Japan.
Chisa NakashimaDepartment of Dermatology, Kyoto University Graduate School of Medicine, 54 Shogoin-Kawara, Sakyo, Kyoto, 606-8507 Japan.
Kenji KabashimaDepartment of Dermatology, Kyoto University Graduate School of Medicine, 54 Shogoin-Kawara, Sakyo, Kyoto, 606-8507 Japan.
Kyoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atopic dermatitis (AD) is a common chronic skin inflammatory disorder characterized by recurrent eczema accompanied by an intractable itch that leads to an impaired quality of life. Extensive recent studies have shed light on the multifaceted pathogenesis of the disease. The complex interplay among skin barrier deficiency, immunological derangement, and pruritus contributes to the development, progression, and chronicity of the disease. Abnormalities in filaggrin, other stratum corneum constituents, and tight junctions induce and/or promote skin inflammation. This inflammation, in turn, can further deteriorate the barrier function by downregulating a myriad of essential barrier-maintaining molecules. Pruritus in AD, which may be due to hyperinnervation of the epidermis, increases pruritogens, and central sensitization compromises the skin integrity and promotes inflammation. There are unmet needs in the treatment of AD. Based on the detailed evidence available to date, certain disease mechanisms can be chosen as treatment targets. Numerous clinical trials of biological agents are currently being conducted and are expected to provide treatments for patients suffering from AD in the future. This review summarizes the etiopathogenesis of the disease and provides a rationale for choosing the novel targeted therapy that will be available in the future.

Indexed as

AdaptiveAtopic dermatitisFilaggrinImmunologyInnatePathogenesis

Identifiers

PMID29259713
PMCPMC5725646
OpenAlexW2623738179

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.