Evidence map›Paper›PMID 37853335›Full record

ArticleBMC nephrology2023

Identifying key genes for diabetic kidney disease by bioinformatics analysis.

Yushan Xu, Lan Li, Ping Tang, Jingrong Zhang, Ruxian Zhong, Jingmei Luo, Jie Lin, Lihua Zhang

Open access · goldAbstract read
In one paragraph

Article in BMC nephrology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.3field-weighted citation impact, top 17% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
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  4. 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

8 authors at 2 institutions in 1 country.

Yushan Xu *Department of Endocrinology, The First Affiliated Hospital of Kunming Medical University, Kunming, 650031, China.
Lan Li *Department of Diabetes, The First Affiliated Hospital of Kunming Medical University, Kunming, 650031, China.
Ping TangDepartment of General Practice, The First Affiliated Hospital of Kunming Medical University, Kunming, 650031, China.
Jingrong ZhangDepartment of General Practice, The First Affiliated Hospital of Kunming Medical University, Kunming, 650031, China.
Ruxian ZhongDepartment of General Practice, The First Affiliated Hospital of Kunming Medical University, Kunming, 650031, China.
Jingmei LuoDepartment of General Practice, The First Affiliated Hospital of Kunming Medical University, Kunming, 650031, China.
Jie LinDepartment of General Practice, The First Affiliated Hospital of Kunming Medical University, Kunming, 650031, China.
Lihua ZhangDepartment of General Practice, The First Affiliated Hospital of Kunming Medical University, Kunming, 650031, China. lihuazhang772002@163.com.
First Affiliated Hospital of Kunming Medical University · CNKunming Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThere are no reliable molecular targets for early diagnosis and effective treatment in the clinical management of diabetic kidney disease (DKD). To identify novel gene factors underlying the progression of DKD.

methodsThe public transcriptomic datasets of the alloxan-induced DKD model and the streptozotocin-induced DKD model were retrieved to perform an integrative bioinformatic analysis of differentially expressed genes (DEGs) shared by two experimental animal models. The dominant biological processes and pathways associated with DEGs were identified through enrichment analysis. The expression changes of the key DEGs were validated in the classic db/db DKD mouse model.

resultsThe downregulated and upregulated genes in DKD models were uncovered from GSE139317 and GSE131221 microarray datasets. Enrichment analysis revealed that metabolic process, extracellular exosomes, and hydrolase activity are shared biological processes and molecular activity is altered in the DEGs. Importantly, Hmgcs2, angptl4, and Slco1a1 displayed a consistent expression pattern across the two DKD models. In the classic db/db DKD mice, Hmgcs2 and angptl4 were also found to be upregulated while Slco1a1 was downregulated in comparison to the control animals.

conclusionsIn summary, we identified the common biological processes and molecular activity being altered in two DKD experimental models, as well as the novel gene factors (Hmgcs2, Angptl4, and Slco1a1) which may be implicated in DKD. Future works are warranted to decipher the biological role of these genes in the pathogenesis of DKD.

Indexed as

Diabetes MellitusDiabetic NephropathiesAnimalsComputational BiologyGene Expression ProfilingMiceDiabetic Kidney Disease (DKD)Differentially Expressed Genes (DEGs)mRNA microarray datasetsPathogenesis

Identifiers

PMID37853335
PMCPMC10585855
OpenAlexW4387764541

What OpenQuestion holds

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Registered trials

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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.