Evidence map›Paper›PMID 37545827›Full record

ArticlePostepy dermatologii i alergologii2023

MiR-125a-3p alleviates hyperproliferation of keratinocytes and psoriasis-like inflammation by targeting TLR4/NF-κB pathway.

Zhao Jin, Qinsi Huang, Jing Peng, Zhong Liu, Rongyi Hu, Juan Wu, Fei Wang

Abstract read
In one paragraph

Article in Postepy dermatologii i alergologii, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
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

8 citing papers in PubMed.

  1. Review
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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

7 authors.

Zhao JinDepartment of Dermatology, Wuhan No. 1 Hospital, Wuhan, Hubei, China.
Qinsi HuangDepartment of Dermatology, Wuhan No. 1 Hospital, Wuhan, Hubei, China.
Jing PengDepartment of Dermatology, Wuhan No. 1 Hospital, Wuhan, Hubei, China.
Zhong LiuDepartment of Dermatology, Wuhan No. 1 Hospital, Wuhan, Hubei, China.
Rongyi HuDepartment of Dermatology, Wuhan No. 1 Hospital, Wuhan, Hubei, China.
Juan WuDepartment of Dermatology, Wuhan No. 1 Hospital, Wuhan, Hubei, China.
Fei WangDepartment of Chinese Medicine, Wuhan No. 1 Hospital, Wuhan, Hubei, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Psoriasis is a chronic auto-inflammatory dermatosis characterized by hyperproliferation of keratinocytes. Emerging evidence has validated the dysregulated expression of microRNAs (miRNAs/miRs) in psoriasis patients. Aim: To probe into the role and precise mechanism of miR-125a-3p in HaCaT cells and imiquimod (IMQ)-stimulated psoriasis-like mice. Material and methods: In M5-treated HaCaT cells and IMQ-stimulated psoriasis-like mice, real-time quantitative polymerase chain reaction and western blot analysis were performed for detecting gene expression. Hematoxylin and eosin staining was used to evaluate pathological morphology of IMQ-induced psoriasis skin. The proliferation of keratinocytes was assessed using Cell Counting Kit-8 assay and Ki67 positive staining. The combination between miR-125a-3p and Toll-like receptor 4 (TLR4) was confirmed by luciferase reporter assay. Results: Our study showed reduced miR-125a-3p expression in psoriasis patients, psoriasis-like inflammatory cell models, and IMQ-generated psoriasis-like mouse models. MiR-125a-3p repressed the activity of keratinocytes Conclusions: Upregulation of miR-125a-3p protects keratinocytes against hyperproliferation and inflammatory damage by inhibiting TLR4, suggesting that the miR-125a-3p/TLR4 axis might become a novel target for the prevention of psoriasis.

Indexed as

hyperproliferationinflammationmiR-125a-3ppsoriasisToll-like receptor 4

Identifiers

PMID37545827
PMCPMC10399661

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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.