Evidence map›Paper›PMID 34654473›Full record

ArticleDiabetology & metabolic syndrome2021

LncRNA KCNQ1OT1 promotes the development of diabetic nephropathy by regulating miR-93-5p/ROCK2 axis.

Li Zhao, Huaqian Chen, Lin Wu, Zhengdong Li, Ren Zhang, Yan Zeng, Tao Yang, Hualing Ruan

Open access · goldAbstract read
In one paragraph

Article in Diabetology & metabolic syndrome, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.9field-weighted citation impact, top 31% 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

11 citing papers in PubMed, 15 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

8 authors at 1 institution in 1 country.

Li ZhaoDepartment of Nephrology, Affiliated Dongfeng Hospital, Hubei University of Medicine, Shiyan, Hubei, People's Republic of China.
Huaqian ChenDepartment of Nephrology, Affiliated Dongfeng Hospital, Hubei University of Medicine, Shiyan, Hubei, People's Republic of China.
Lin WuDepartment of Nephrology, Sinopharm Hanjiang Hospital, Hubei University of Medicine, Shiyan, Hubei, People's Republic of China.
Zhengdong LiDepartment of Nephrology, Affiliated Dongfeng Hospital, Hubei University of Medicine, Shiyan, Hubei, People's Republic of China.
Ren ZhangDepartment of Nephrology, Affiliated Dongfeng Hospital, Hubei University of Medicine, Shiyan, Hubei, People's Republic of China.
Yan ZengDepartment of Nephrology, Affiliated Dongfeng Hospital, Hubei University of Medicine, Shiyan, Hubei, People's Republic of China.
Tao YangDepartment of Nephrology, Affiliated Dongfeng Hospital, Hubei University of Medicine, Shiyan, Hubei, People's Republic of China.
Hualing RuanDepartment of Endocrinology, Zhangwan District, Affiliated Dongfeng Hospital, Hubei University of Medicine, No. 16 Daling Road, Shiyan, Hubei, China. rhqnscr@163.com.
Hubei University of Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLong non-coding RNAs (lncRNAs) have been reported to play vital roles in diabetic nephropathy (DN). The aim of this study was to explore the function of mechanism of lncRNA KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1) in DN.

methodsDN cell models were established using high glucose (HG) treatment in human glomerular mesangial cells (HGMC) and human renal glomerular endothelial cells (HRGEC). The expression levels of KCNQ1OT1, microRNA-93-5p (miR-93-5p), and Rho associated coiled-coil containing protein kinase 2 (ROCK2) mRNA was detected by quantitative real-time polymerase chain reaction (qRT-PCR). Cell Counting Kit-8 (CCK-8) assay and flow cytometry were used to detect cell proliferation and apoptosis, respectively. ROCK2 and apoptosis/fibrosis-related protein levels were examined by western blot. The predicted interaction between miR-93-5p and KCNQ1OT1 or ROCK2 was verified by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay.

resultsKCNQ1OT1 was upregulated in DN patients and DN cell models. KCNQ1OT1 knockdown inhibited cell proliferation and fibrosis and induced apoptosis in DN cell models. MiR-93-5p was a direct target of KCNQ1OT1, and miR-93-5p inhibition restored the KCNQ1OT1 knockdown-mediated effects on cell proliferation, fibrosis and apoptosis in DN cell models. In addition, ROCK2 was identified as a target of miR-93-5p, and miR-93-5p overexpression suppressed cell proliferation and fibrosis and accelerated apoptosis by targeting ROCK2 in DN cell models. Moreover, KCNQ1OT1 regulated ROCK2 expression by binding to miR-93-5p.

conclusionKCNQ1OT1 knockdown inhibited cell proliferation and fibrosis and induced apoptosis in DN by regulating miR-93-5p/ROCK2 axis, providing potential value for the treatment of DN.

Indexed as

Diabetic nephropathyKCNQ1OT1miR-93-5pROCK2

Identifiers

PMID34654473
PMCPMC8518197
OpenAlexW3206794952

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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.