Evidence map›Paper›PMID 30180910›Full record

ArticleBiological research2018

miR-214 ameliorates acute kidney injury via targeting DKK3 and activating of Wnt/β-catenin signaling pathway.

Xiaoguang Zhu, Wenwen Li, Huicong Li

Open access · goldAbstract read
In one paragraph

Article in Biological research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 5% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.

  1. Pooled it
  2. Review
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  4. Silencing circ_0074371 inhibits the progression of sepsis-induced acute kidney injury by regulating miR-330-5p/ELK1 axis.Mammalian genome : official journal of the International Mammalian Genome Society · 2022
    Article
  5. MicroRNAs in kidney injury and disease.Nature reviews. Nephrology · 2022
    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

3 authors at 1 institution in 1 country.

Xiaoguang ZhuDepartment of Nephrology, Huaihe Hospital of Henan University, No. 8, Baobei Road, Gulou District, Kaifeng, 475000, China. zhuxiaoguangzxg@sina.com.ORCID http://orcid.org/0000-0001-5599-8785
Wenwen LiDepartment of Cardiology, Huaihe Hospital of Henan University, Kaifeng, 475000, China.
Huicong LiDepartment of Nephrology, Huaihe Hospital of Henan University, No. 8, Baobei Road, Gulou District, Kaifeng, 475000, China.
Henan University Huaihe Hospital and Huaihe Clinical Institute · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundmiR-214 was demonstrated to be upregulated in models of renal disease and promoted fibrosis in renal injury independent of TGF-β signaling in vivo. However, the detailed role of miR-214 in acute kidney injury (AKI) and its underlying mechanism are still largely unknown.

methodsIn this study, an I/R-induced rat AKI model and a hypoxia-induced NRK-52E cell model were used to study AKI. The concentrations of kidney injury markers serum creatinine, blood urea nitrogen, and kidney injury molecule-1 were measured. The expressions of miR-214, tumor necrosis factor-α, interleukin (IL)-1β, IL-6, were detected by RT-qPCR. The protein levels of Bcl-2, Bax, Dickkopf-related protein 3, β-catenin, c-myc, and cyclinD1 were determined by western blot. Cell apoptosis and caspase 3 activity were evaluated by flow cytometry analysis and caspase 3 activity assay, respectively. Luciferase reporter assay was used to confirm the interaction between miR-214 and Dkk3.

resultsmiR-214 expression was induced in ischemia-reperfusion (I/R)-induced AKI rat and hypoxic incubation of NRK-52E cells. Overexpression of miR-214 alleviated hypoxia-induced NRK-52E cell apoptosis while inhibition of miR-214 expression exerted the opposite effect. Dkk3 was identified as a target of miR-214. Anti-miR-214 abolished the inhibitory effects of DKK3 knockdown on hypoxia-induced NRK-52E cell apoptosis by inactivation of Wnt/β-catenin signaling. Moreover, miR-214 ameliorated AKI in vivo by inhibiting apoptosis and fibrosis through targeting Dkk3 and activating Wnt/β-catenin pathway.

conclusionmiR-214 ameliorates AKI by inhibiting apoptosis through targeting Dkk3 and activating Wnt/β-catenin signaling pathway, offering the possibility of miR-214 in the therapy of ischemic AKI.

Indexed as

Acute Kidney InjuryAdaptor Proteins, Signal TransducingAnimalsCateninsCell ProliferationChemokinesDisease Models, AnimalIntercellular Signaling Peptides and ProteinsMaleMicroRNAsRatsRats, Sprague-DawleyWnt Signaling PathwayAdaptor Proteins, Signal TransducingCateninsChemokinesDKK3 protein, humanIntercellular Signaling Peptides and ProteinsMicroRNAsAcute kidney injuryDkk3miR-214Wnt/β-catenin signaling pathway

Identifiers

PMID30180910
PMCPMC6122444
OpenAlexW2892185452

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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.