Evidence map›Paper›PMID 31746345›Full record

ArticleInternational journal of molecular medicine2020

miRNA‑342 suppresses renal interstitial fibrosis in diabetic nephropathy by targeting SOX6.

Zhen-Huan Jiang, Yun-Zhao Tang, Hong-Na Song, Min Yang, Bin Li, Chang-Lin Ni

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

47 citing papers in PubMed, 71 citations in OpenAlex.

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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.

Zhen-Huan JiangNHC Key Laboratory of Hormones and Development, Tianjin Key Laboratory of Metabolic Diseases, Tianjin Medical University Chu Hsien‑I Memorial Hospital and Tianjin Institute of Endocrinology, Tianjin 300134, P.R. China.
Yun-Zhao TangNHC Key Laboratory of Hormones and Development, Tianjin Key Laboratory of Metabolic Diseases, Tianjin Medical University Chu Hsien‑I Memorial Hospital and Tianjin Institute of Endocrinology, Tianjin 300134, P.R. China.
Hong-Na SongNHC Key Laboratory of Hormones and Development, Tianjin Key Laboratory of Metabolic Diseases, Tianjin Medical University Chu Hsien‑I Memorial Hospital and Tianjin Institute of Endocrinology, Tianjin 300134, P.R. China.
Min YangNHC Key Laboratory of Hormones and Development, Tianjin Key Laboratory of Metabolic Diseases, Tianjin Medical University Chu Hsien‑I Memorial Hospital and Tianjin Institute of Endocrinology, Tianjin 300134, P.R. China.
Bin LiNHC Key Laboratory of Hormones and Development, Tianjin Key Laboratory of Metabolic Diseases, Tianjin Medical University Chu Hsien‑I Memorial Hospital and Tianjin Institute of Endocrinology, Tianjin 300134, P.R. China.
Chang-Lin NiNHC Key Laboratory of Hormones and Development, Tianjin Key Laboratory of Metabolic Diseases, Tianjin Medical University Chu Hsien‑I Memorial Hospital and Tianjin Institute of Endocrinology, Tianjin 300134, P.R. China.
Tianjin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic kidney disease (DKD) is one of the major microvascular complications in patients with type 1 and/or type 2 diabetes, the first cause of end‑stage renal disease (ESRD) in several countries and regions. However, the pathogenesis of DKD and the mechanisms through which it leads to ESRD remain unknown. Thus, in this study, we aimed to elucidate some of these mechanisms. The expression of microRNA (miRNA or miR)‑342‑3p and SRY‑box 6 (SOX6) in the renal tissues of mice with DKD and mouse renal mesangial cells (MCs) was determined by RT‑qPCR and western blot analysis. The diabetic kidney environment was established using high‑glucose medium. SOX6 was verified as a target gene of miR‑342‑3p by dual‑luciferase activity assay. In addition, western blot analysis was employed to determine the changes in the levels of several biomarkers of fibrosis [transforming growth factor (TGF)‑β1, fibronectin (FN), collagen IV (referred to as C‑IV) and phosphatase and tensin homolog (PTEN)]. Compared with THE control mice, the expression of miR‑342‑3p in the kidney tissues of mice with DKD was downregulated, whereas that of SOX6 was upregulated. The same phenomenon was observed in the MCs cultured in high‑glucose medium. Subsequently, miR‑342‑3p inhibited SOX6 expression, promoted cell proliferation and inhibited the apoptosis of MCs. Moreover, the overexpression of miR‑342‑3p suppressed high glucose‑induced renal interstitial fibrosis. In addition, it was found that miR‑342‑3p inhibited SOX6 expression by binding to the 3'‑UTR of SOX6. On the whole, the findings of this study demonstrate that miR‑342‑3p suppresses the progression of DKD by inducing the degradation of SOX6. Thus, the miR‑342‑3p/SOX6 axis may serve as a novel therapeutic target in the treatment of DKD.

Indexed as

Gene Expression RegulationRNA Interference3' Untranslated RegionsAnimalsApoptosisBiomarkersBlood GlucoseCell ProliferationDiabetic NephropathiesFibrosisGenes, ReporterMaleMesangial CellsMiceMicroRNAsSOXD Transcription Factors3' Untranslated RegionsBiomarkersBlood GlucoseMicroRNAsMIRN342 microRNA, humanSOX6 protein, humanSOXD Transcription Factorsdiabetic kidney diseasemicroRNA-342-3prenal interstitial fibrosisSOX6

Identifiers

PMID31746345
PMCPMC6889927
OpenAlexW2986052625

What OpenQuestion holds

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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 OpenQuestion graph.