Evidence map›Paper›PMID 35392987›Full record

ArticleEuropean journal of medical research2022

Knockdown of circ_0003928 ameliorates high glucose-induced dysfunction of human tubular epithelial cells through the miR-506-3p/HDAC4 pathway in diabetic nephropathy.

Qiong Liu, Yuanyuan Cui, Nan Ding, Changxue Zhou

Open access · goldAbstract read
In one paragraph

Article in European journal of medical research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

20 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
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  5. Histone deacetylases and their inhibitors in kidney diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
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  19. Epigenetic modification in diabetic kidney disease.Frontiers in endocrinology · 2023
    Review
  20. The role of circular RNA in Diabetic Nephropathy.International journal of medical sciences · 2022
    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

4 authors at 2 institutions in 1 country.

Qiong LiuDepartment of Nephrology, Hebei General Hospital, Shijiazhuang, China.
Yuanyuan CuiDepartment of Endocrine Rheumatology and Immunology, People's Hospital of Gaotang County, Gaotang, China.
Nan DingDepartment of Clinical Laboratory, Hebei General Hospital, Shijiazhuang, China.
Changxue ZhouDepartment of Kidney Internal Medicine, Zaozhuang Municipal Hospital, No. 41 Longtou Road, Central District, Zaozhuang, 277100, China. changxuezhou@163.com.
Hebei General Hospital · CNZaozhuang Municipal Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPrevious data have indicated the importance of circular RNA (circRNA) in the pathogenesis of diabetic nephropathy (DN). The study is designed to investigate the effects of circ_0003928 on oxidative stress and apoptosis of high glucose (HG)-treated human tubular epithelial cells (HK-2) and the underlying mechanism.

methodsThe DN cell model was established by inducing HK-2 cells using 30 mmol/L D-glucose. RNA expression of circ_0003928, miR-506-3p and histone deacetylase 4 (HDAC4) was detected by quantitative real-time polymerase chain reaction. Cell viability and proliferation were investigated by cell counting kit-8 and 5-Ethynyl-29-deoxyuridine (EdU) assays, respectively. Oxidative stress was evaluated by commercial kits. Caspase 3 activity and cell apoptotic rate were assessed by a caspase 3 activity assay and flow cytometry analysis, respectively. Protein expression was detected by Western blotting analysis. The interactions among circ_0003928, miR-506-3p and HDAC4 were identified by dual-luciferase reporter and RNA pull-down assays.

resultsCirc_0003928 and HDAC4 expression were significantly upregulated, while miR-506-3p was downregulated in the serum of DN patients and HG-induced HK-2 cells. HG treatment inhibited HK-2 cell proliferation, but induced oxidative stress and cell apoptosis; however, these effects were reversed after circ_0003928 depletion. Circ_0003928 acted as a miR-506-3p sponge, and HDAC4 was identified as a target gene of miR-506-3p. Moreover, the circ_0003928/miR-506-3p/HDAC4 axis regulated HG-induced HK-2 cell dysfunction.

conclusionCirc_0003928 acted as a sponge for miR-506-3p to regulate HG-induced oxidative stress and apoptosis of HK-2 cells through HDAC4, which suggested that circ_0003928 might be helpful in the therapy of DN.

Indexed as

Diabetes MellitusDiabetic NephropathiesMicroRNAsApoptosisCaspase 3Epithelial CellsGlucoseHistone DeacetylasesHumansRepressor ProteinsCaspase 3GlucoseHDAC4 protein, humanHistone DeacetylasesMicroRNAsMIRN506 microRNA, humanRepressor Proteinscirc_0003928DNHDAC4miR-506-3p

Identifiers

PMID35392987
PMCPMC8991937
OpenAlexW4223425780

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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.