Evidence map›Paper›PMID 32235789›Full record

ArticleInternational journal of molecular sciences2020

Role of Aryl Hydrocarbon Receptor Activation and Autophagy in Psoriasis-Related Inflammation.

Hye Ran Kim, Seok Young Kang, Hye One Kim, Chun Wook Park, Bo Young Chung

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

26 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. How Cells Die in Psoriasis?International journal of molecular sciences · 2025
    Review
  6. The Aryl Hydrocarbon Receptor (AHR): Peacekeeper of the Skin.International journal of molecular sciences · 2025
    Review
  7. Review
  8. Review
  9. A Snapshot of Biomarkers in Psoriasis.Current drug discovery technologies · 2025
    Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
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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

5 authors at 1 institution in 1 country.

Hye Ran KimDepartment of Dermatology, Hallym University Kangnam Sacred Heart Hospital, Hallym University College of Medicine, Seoul 07441, Korea.ORCID 0000-0001-7519-8910
Seok Young KangDepartment of Dermatology, Hallym University Kangnam Sacred Heart Hospital, Hallym University College of Medicine, Seoul 07441, Korea.
Hye One KimDepartment of Dermatology, Hallym University Kangnam Sacred Heart Hospital, Hallym University College of Medicine, Seoul 07441, Korea.
Chun Wook ParkDepartment of Dermatology, Hallym University Kangnam Sacred Heart Hospital, Hallym University College of Medicine, Seoul 07441, Korea.
Bo Young ChungDepartment of Dermatology, Hallym University Kangnam Sacred Heart Hospital, Hallym University College of Medicine, Seoul 07441, Korea.
Hallym University Kangnam Sacred Heart Hospital · KR

Funding

Hallym University Research Fund HURF-2019-72National Research Foundation of Korea (NRF) 2018R1C1B6007998
6 · The paper itself

Abstract

Aryl hydrocarbon receptor (AhR) and autophagy reportedly regulate immune responses in the skin. This study explored the effects of AhR activation on autophagy in human keratinocytes, and the relevance of AhR and autophagy in psoriasis pathogenesis. AhR activation by 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) repressed autophagy, while autophagy inhibition induced AhR activation in HaCaT cells and normal human epidermal keratinocytes (NHEKs). A particularly strong interaction between AhR and autophagy was observed in proinflammatory cytokines-stimulated keratinocytes, an in vitro model of psoriasis. In skin biopsies from psoriasis patients, a similar impact of AhR on autophagy and inflammation was observed. AhR inhibition blocked TCDD- and chloroquine-induced p65NF-κB and p38MAPK phosphorylation in proinflammatory cytokines-stimulated HaCaT cells. Moreover, higher expression of AhR and CYP1A1, and lower expression of LC3, were detected in psoriatic skin tissues, compared to the controls. These data demonstrated that AhR modulated autophagy leads to skin inflammation in human keratinocytes via the p65NF-κB/p38MAPK signaling pathways, suggesting that AhR signaling and autophagy might be involved in the pathogenesis of chronic inflammatory disorders such as psoriasis.

Indexed as

AutophagyAnimalsBasic Helix-Loop-Helix ProteinsCell LineCells, CulturedHumansInflammationKeratinocytesPsoriasisReceptors, Aryl HydrocarbonSkinAHR protein, humanBasic Helix-Loop-Helix ProteinsReceptors, Aryl Hydrocarbon2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD)aryl hydrocarbon receptorautophagypsoriasisskin

Identifiers

PMID32235789
PMCPMC7139675
OpenAlexW3012657936

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.