Evidence map›Paper›PMID 34486983›Full record

ArticleEndocrine connections2021

A bioinformatics analysis of the contribution of m6A methylation to the occurrence of diabetes mellitus.

Lei Lei, Yi-Hua Bai, Hong-Ying Jiang, Ting He, Meng Li, Jia-Ping Wang

Open access · goldAbstract read
In one paragraph

Article in Endocrine connections, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

7 citing papers in PubMed, 14 citations in OpenAlex.

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  7. Alteration of mFrontiers in neuroscience · 2022
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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

6 authors at 1 institution in 1 country.

Lei LeiDepartment of Nephrology, The Second Hospital Affiliated to Kunming Medical University, Kunming, Yunnan, China.
Yi-Hua BaiDepartment of Nephrology, The Second Hospital Affiliated to Kunming Medical University, Kunming, Yunnan, China.
Hong-Ying JiangDepartment of Nephrology, The Second Hospital Affiliated to Kunming Medical University, Kunming, Yunnan, China.
Ting HeDepartment of Nephrology, The Second Hospital Affiliated to Kunming Medical University, Kunming, Yunnan, China.
Meng LiDepartment of Nephrology, The Second Hospital Affiliated to Kunming Medical University, Kunming, Yunnan, China.
Jia-Ping WangDepartment of Radiology, The Second Hospital Affiliated to Kunming Medical University, Kunming, Yunnan, China.
Kunming Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

N6-methyladenosine (m6A) methylation has been reported to play a role in type 2 diabetes (T2D). However, the key component of m6A methylation has not been well explored in T2D. This study investigates the biological role and the underlying mechanism of m6A methylation genes in T2D. The Gene Expression Omnibus (GEO) database combined with the m6A methylation and transcriptome data of T2D patients were used to identify m6A methylation differentially expressed genes (mMDEGs). Ingenuity pathway analysis (IPA) was used to predict T2D-related differentially expressed genes (DEGs). Gene ontology (GO) term enrichment and the Kyoto Encyclopedia of Genes and Genomes (KEGG) were used to determine the biological functions of mMDEGs. Gene set enrichment analysis (GSEA) was performed to further confirm the functional enrichment of mMDEGs and determine candidate hub genes. The least absolute shrinkage and selection operator (LASSO) regression analysis was carried out to screen for the best predictors of T2D, and RT-PCR and Western blot were used to verify the expression of the predictors. A total of 194 overlapping mMDEGs were detected. GO, KEGG, and GSEA analysis showed that mMDEGs were enriched in T2D and insulin signaling pathways, where the insulin gene (INS), the type 2 membranal glycoprotein gene (MAFA), and hexokinase 2 (HK2) gene were found. The LASSO regression analysis of candidate hub genes showed that the INS gene could be invoked as a predictive hub gene for T2D. INS, MAFA,and HK2 genes participate in the T2D disease process, but INS can better predict the occurrence of T2D.

Indexed as

bioinformaticsHK2INSMAFAN6-methyladenosine methylationtype 2 diabetes

Identifiers

PMID34486983
PMCPMC8558884
OpenAlexW3198602357

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.