Evidence map›Paper›PMID 32073611›Full record

ArticleBioscience reports2020

MicroRNA-140-5p ameliorates the high glucose-induced apoptosis and inflammation through suppressing TLR4/NF-κB signaling pathway in human renal tubular epithelial cells.

Jie Su, Jian Ren, Haiyan Chen, Bo Liu

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Bioscience reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 2 pooled it
2.5field-weighted citation impact, top 9% 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

28 citing papers in PubMed, 2 syntheses or guidelines pooled it, 46 citations in OpenAlex.

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  16. Role of renal tubular programed cell death in diabetic kidney disease.Diabetes/metabolism research and reviews · 2023
    Review
  17. Epigenetic regulation of Toll-like receptors 2 and 4 in kidney disease.Journal of molecular medicine (Berlin, Germany) · 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

4 authors at 3 institutions in 1 country.

Jie SuDepartment of Endocrinology, Luoyang Central Hospital Affiliated to ZhengZhou University, Luoyang 471000, Henan, China.
Jian RenDepartment of Endocrinology, Zhengzhou Central Hospital Affiliated to ZhengZhou University, Zhengzhou 450000, Henan, China.
Haiyan ChenDepartment of Endocrinology, Luoyang Central Hospital Affiliated to ZhengZhou University, Luoyang 471000, Henan, China.
Bo LiuDepartment of Neurosurgery, 150th Central Hospital of Chinese People's Liberation Army, Luoyang 471000, Henan, China.
Luoyang Central Hospital Affiliated to Zhengzhou University · CNPeople's Liberation Army No. 150 Hospital · CNZhengzhou Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hyperglycemia-induced renal tubular cell injury is thought to play a critical role in the pathogenesis of diabetic nephropathy (DN). However, the role of miRNAs in renal tubular cell injury remains to be fully elucidated. The aim of the present study was to investigate the role and mechanisms of miRNAs protecting against high glucose (HG)-induced apoptosis and inflammation in renal tubular cells. First, we analyzed microRNA (miRNA) expression profiles in kidney tissues from DN patients using miRNA microarray. It was observed that miRNA-140-5p (miR-140-5p) was significantly down-regulated in kidney tissues from patients with DN. An inverse correlation between miR-140-5p expression levels with serum proteinuria was observed in DN patients, suggesting miR-140-5p may be involved in the progression of DN. HG-induced injury in HK-2 cells was used to explore the potential role of miR-140-5p in DN. We found that miR-140-5p overexpression improved HG-induced cell injury, as evidenced by the enhancement of cell viability, and inhibition of the activity of caspase-3 and reactive oxygen species (ROS) generation. It was also observed that up-regulation of miR-140-5p suppressed HG induced the expressions of pro-inflammatory cytokines, such as tumor necrosis factor-α (TNF-α), interleukin (IL)-1β and IL-6 in HK-2 cells. In addition, TLR4, one of the upstream molecules of NF-κB signaling pathway, was found to be a direct target of miR-140-5p in the HK-2. Moreover, the HG-induced activation of NF-κB signaling pathway was inhibited by miR-140-5p overexpression. These results indicated that miR-140-5p protected HK-2 cells against HG-induced injury through blocking the TLR4/NF-κB pathway, and miR-140-5p may be considered as a potential prognostic biomarker and therapeutic target in the treatment of DN.

Indexed as

AdultAgedApoptosisCell SurvivalChinaDiabetic NephropathiesEpithelial CellsFemaleGene ExpressionGene Expression ProfilingGlucoseHumansKidneyKidney TubulesMaleMicroRNAsGlucoseMicroRNAsMirn140 microRNA, humanNF-kappa BToll-Like Receptor 4apoptosisdiabetic nephropathymicroRNA-140-5ppro–inflammatory cytokinesrenal tubular cellTLR4/NF-κB pathway

Identifiers

PMID32073611
PMCPMC7056448
OpenAlexW3007734365

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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.