Evidence map›Paper›PMID 33911791›Full record

ArticleAnnals of dermatology2020

Possible Role of Lysine Demethylase 2A in the Pathophysiology of Psoriasis.

Dong Ha Kim, Mi-Ra Choi, Jae Kyung Lee, Dong-Kyun Hong, Kyung Eun Jung, Chong Won Choi, Young Lee, Chang-Deok Kim, Young-Joon Seo, Jeung-Hoon Lee

Open access · diamondAbstract read
In one paragraph

Article in Annals of dermatology, 2020. 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
0.2field-weighted citation impact, top 46% 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

4 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Histone demethylases in autophagy and inflammation.Cell communication and signaling : CCS · 2025
    Review
  3. Article
  4. Article
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.

Dong Ha KimDepartment of Dermatology, School of Medicine, Chungnam National University, Daejeon, Korea.ORCID https://orcid.org/0000-0002-0676-6547
Mi-Ra ChoiDepartment of Dermatology, School of Medicine, Chungnam National University, Daejeon, Korea.ORCID https://orcid.org/0000-0003-0734-8360
Jae Kyung LeeDepartment of Dermatology, School of Medicine, Chungnam National University, Daejeon, Korea.ORCID https://orcid.org/0000-0002-9922-5730
Dong-Kyun HongDepartment of Dermatology, School of Medicine, Chungnam National University, Daejeon, Korea.ORCID https://orcid.org/0000-0002-4244-0691
Kyung Eun JungDepartment of Dermatology, School of Medicine, Chungnam National University, Daejeon, Korea.ORCID https://orcid.org/0000-0003-0968-1079
Chong Won ChoiDepartment of Dermatology, School of Medicine, Chungnam National University, Daejeon, Korea.ORCID https://orcid.org/0000-0001-9994-8819
Young LeeDepartment of Dermatology, School of Medicine, Chungnam National University, Daejeon, Korea.ORCID https://orcid.org/0000-0001-9205-1785
Chang-Deok KimDepartment of Dermatology, School of Medicine, Chungnam National University, Daejeon, Korea.ORCID https://orcid.org/0000-0001-9341-6491
Young-Joon SeoDepartment of Dermatology, School of Medicine, Chungnam National University, Daejeon, Korea.ORCID https://orcid.org/0000-0002-4955-590X
Jeung-Hoon LeeDepartment of Dermatology, School of Medicine, Chungnam National University, Daejeon, Korea.ORCID https://orcid.org/0000-0002-4869-940X
Chungnam National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPsoriasis is a common chronic inflammatory skin disease. The development of psoriasis is dependent on many intercellular events such as innate immunity and T cell-mediated inflammation. Furthermore, genetic factors are strongly implicated in the pathophysiology of psoriasis. Although a variety of susceptible genes are identified, it is likely that many important genes remain undisclosed.

objectiveThe aim of this study is to investigate the possible role of lysine demethylase 2A (KDM2A) in the pathophysiology of psoriasis.

methodsWe examined the expression of KDM2A using a well established imiquimod-induced psoriasiform dermatitis model.

resultsImmunohistochemistry analysis showed that expression of KDM2A was increased in imiquimod-induced psoriasiform dermatitis. Consistent with this result, KDM2A level was markedly increased in the epidermis of psoriatic patient. When keratinocytes were stimulated with TLR3 agonist poly(I:C), KDM2A was increased at both the mRNA and protein levels. Poly(I:C) increased the expression of psoriasis-related cytokines including tumor necrosis factor-α, interleukin-8, and CCL20, and KDM2A inhibitor daminozide enhanced the poly(I:C)-induced cytokine expression. Finally, topical co-application of imiquimod and daminozide exacerbated the imiquimod-induced psoriasiform dermatitis.

conclusionTogether, these results suggest that KDM2A is increased to negatively regulate the inflammatory reaction of epidermal keratinocytes in psoriasis.

Indexed as

ImiquimodKeratinocytesLysine demethylase 2APolyinosinic: polycytidylic acidPsoriasis

Identifiers

PMID33911791
PMCPMC7875244
OpenAlexW3098473564

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.