Evidence map›Paper›PMID 33948156›Full record

ArticleTherapeutic advances in chronic disease2021

EZH2 is involved in psoriasis progression by impairing miR-125a-5p inhibition of SFMBT1 and leading to inhibition of the TGFβ/SMAD pathway.

Shengming Qu, Zhe Liu, Bing Wang

Open access · goldAbstract read
In one paragraph

Article in Therapeutic advances in chronic disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Emerging roles of non-coding RNAs in psoriasis pathogenesis.Functional & integrative genomics · 2023
    Review
  9. Article
  10. Article
  11. Mouse Models of Psoriasis: A Comprehensive Review.The Journal of investigative dermatology · 2022
    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

3 authors at 1 institution in 1 country.

Shengming QuDepartment of Dermatology, The Second Hospital of Jilin University, Changchun, P.R. China.
Zhe LiuDepartment of Dermatology, The Second Hospital of Jilin University, Changchun, P.R. China.
Bing WangDepartment of Dermatology, The Second Hospital of Jilin University, No. 218, Ziqiang Road, Changchun, Jilin Province 130041, P.R. China.ORCID https://orcid.org/0000-0001-9544-6352
Second Affiliated Hospital of Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsIn this study, we aimed to decipher the impact of enhancer of zeste homolog 2 (EZH2) in psoriasis as well as the underlying mechanism.

methodsA mouse model of psoriasis was developed by means of imiquimod induction, with the expression of EZH2, microRNA-125a-5p (miR-125a-5p), and SFMBT1 determined. The role of EZH2, miR-125a-5p, and SFMBT1 in malignant phenotypes of HaCaT cells and the development of psoriasis

resultsOverexpressed SFMBT1 and EZH2 was detected while miR-125a-5p were downregulated in psoriasis tissues and human keratinocyte (HaCaT) cells. EZH2 increased the levels of IL-17A-induced cytokines and promoted the malignant phenotypes of HaCaT cells. Functionally, EZH2 reduced miR-125a-5p expression while miR-125a-5p targeted SFMBT1 to activate the TGFβ/SMAD pathway

conclusionTaken together, the results of the current study highlight the ability of EZH2 to potentially inactivate the TGFβ/SMAD pathway

Indexed as

EZH2microRNA-125a-5ppsoriasisSFMBT1TGFβ/SMAD pathway

Identifiers

PMID33948156
PMCPMC8053822
OpenAlexW3156386248

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.