Evidence map›Paper›PMID 36195304›Full record

ArticleJornal de pediatria

The immunogenic involvement of miRNA-492 in mycoplasma pneumoniae infection in pediatric patients.

Zhiyi Jia, Qiwei Sun, Yanfei Zheng, Jing Xu, Yanxia Wang

Open access · goldAbstract read
In one paragraph

Article in Jornal de pediatria. 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
1.7field-weighted citation impact, top 15% 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, 11 citations in OpenAlex.

  1. Article
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  7. Biomarkers associated with the diagnosis and prognosis ofFrontiers in cellular and infection microbiology · 2025
    Review
  8. 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.

Zhiyi JiaDepartment of Pediatrics, Zibo Central Hospital, Shandong, China.
Qiwei SunDepartment of Pediatrics, Zibo Central Hospital, Shandong, China. Electronic address: ziboerke1982@163.com.
Yanfei ZhengDepartment of Pediatrics, Zibo Central Hospital, Shandong, China.
Jing XuDepartment of Pediatrics, Zibo Central Hospital, Shandong, China.
Yanxia WangDepartment of Pediatrics, Zibo Central Hospital, Shandong, China.
Central Hospital of Zibo · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThis study aimed to evaluate the role of miRNA-492 in the progression of mycoplasma pneumoniae (MP) infection in pediatric patients.

methodsForty-six children admitted to the present study's hospital and diagnosed with mycoplasma pneumonia were recruited as the study group from March 2018 to August 2019, and 40 healthy children were selected as the control group.

resultsThe expression levels of miRNA-492, TNF-α, IL-6 and IL-18 in the study group were significantly higher than those in the control group (p < 0.05). There was no significant correlation between miRNA-492 and most of the immune-correlated indicators in the study group, except for IL-6, IL-18 and HMGB1. Meanwhile, overexpression of miRNA-492 increased IL-6 secretion in PMA-activated monocytes (p < 0.01).

conclusionThe present study's results suggested that miRNA-492 might play a role in the pathogenesis of mycoplasma pneumoniae pneumonia in children by regulating the secretion of immune-inflammatory factors such as IL-6 and IL-18 in the mononuclear macrophages.

Indexed as

MicroRNAsPneumonia, MycoplasmaChildHumansInterleukin-18Interleukin-6Mycoplasma pneumoniaeInterleukin-18Interleukin-6MicroRNAsHMGB1IL-18IL-6Inflammatory responsesmiRNA-492Mycoplasma pneumoniae pneumonia (MPP)

Identifiers

PMID36195304
PMCPMC10031331
OpenAlexW4298620998

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.