Evidence map›Paper›PMID 35712865›Full record

ArticleJournal of clinical laboratory analysis2022

The downregulation of miR-22 and miR-372 may contribute to gestational diabetes mellitus through regulating glucose metabolism via the PI3K/AKT/GLUT4 pathway.

Wei Li, Xianlin Yuan, Xin He, Li Yang, Yingyuan Wu, Xiaofeng Deng, Yiwen Zeng, Kesheng Hu, Bo Tang

Open access · goldAbstract read
In one paragraph

Article in Journal of clinical laboratory analysis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

12 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
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  9. The role of microRNAs in pregnancies complicated by maternal diabetes.Clinical science (London, England : 1979) · 2024
    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

9 authors at 5 institutions in 1 country.

Wei LiDepartment of Endocrinology, Armed Police Corps Hospital of Guangdong Province, Guangzhou, China.
Xianlin YuanDepartment of Food and Biological Engineering, Guangdong Industry Technical College, Guangzhou, China.ORCID https://orcid.org/0000-0002-5773-852X
Xin HeDepartment of Anesthesiology, Xiangya Hospital, Central South University, Changsha, China.
Li YangDepartment of Endocrinology, Armed Police Corps Hospital of Guangdong Province, Guangzhou, China.
Yingyuan WuDepartment of Obstetrics and Gynecology, Armed Police Corps Hospital of Guangdong Province, Guangzhou, China.
Xiaofeng DengDepartment of Central Sterile Supply, Armed Police Corps Hospital of Guangdong Province, Guangzhou, China.
Yiwen ZengDepartment of Endocrinology, Armed Police Corps Hospital of Guangdong Province, Guangzhou, China.
Kesheng HuDepartment of Clinical Laboratory, Armed Police Corps Hospital of Guangdong Province, Guangzhou, China.
Bo TangDepartment of Clinical Pharmacy, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
JiangSu Armed Police General Hospital · CNGuangdong Police College · CNCentral South University · CNGuangdong Industry Technical College · CNSecond Affiliated Hospital of Guangzhou Medical University · CN

Funding

Guangdong Science and Technology Department 2018A030313556
6 · The paper itself

Abstract

backgroundIdentifying effective regulatory mechanisms will be significant for Gestational diabetes mellitus (GDM) diagnosis and treatment.

methodsThe expressions of miR-22 and miR-372 in placenta tissues from 75 pregnant women with GDM and 75 matched healthy controls and HRT8/SVneo cells (a model of insulin resistance) were analyzed by qPCR. The expressions of PI3K, AKT, IRS, and GLUT4 in high glucose-treated HRT8/SVneo cells transfected with miR-22 or miR-372 mimics or inhibitors was assessed by Western blot. A luciferase gene reporter assay was employed to verify miRNAs' target genes.

resultsThe expressions of miR-22 and miR-372 in placental tissues from GDM patients and HRT8/SVneo cells were significantly decreased compared with the respective controls. The GLUT4 expression was significantly decreased in the placenta tissues of GDM and HRT8/SVneo cells with high glucose transfected with miR-22 and miR-372 inhibitors. We confirmed that SLC2A4, the gene encoding GLUT4, was a direct target of miR-22 and miR-372. In this study, we report that the lower expressions of miR-22 and miR-372 in placental tissue from GDM patients.

conclusionOur results further suggested that the downregulations of miR-22 and miR-372 may contribute to GDM through regulating the PI3K/GLUT4 pathway.

Indexed as

Diabetes, GestationalMicroRNAsDown-RegulationFemaleGlucoseGlucose Transporter Type 4HumansPhosphatidylinositol 3-KinasesPlacentaPregnancyProto-Oncogene Proteins c-aktGlucoseGlucose Transporter Type 4MicroRNAsMIRN22 microRNA, humanMIRN372 microRNA, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSLC2A4 protein, humangestational diabetes mellitusglucose metabolismGLUT4miR-22miR-372

Identifiers

PMID35712865
PMCPMC9279990
OpenAlexW4283033164

What OpenQuestion holds

Textmetadata
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.