Evidence map›Paper›PMID 30729676›Full record

ArticleJournal of cellular and molecular medicine2019

MiR-802 causes nephropathy by suppressing NF-κB-repressing factor in obese mice and human.

Da Sun, Jia Chen, Wei Wu, Ju Tang, Li Luo, Kun Zhang, Libo Jin, Sue Lin, Yitian Gao, Xiaoqing Yan and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 2 pooled it
1.4field-weighted citation impact, top 22% 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

25 citing papers in PubMed, 2 syntheses or guidelines pooled it, 33 citations in OpenAlex.

  1. Pooled it
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  12. miR-802-5p is a key regulator in diabetic kidney disease.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2023
    Article
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  16. Role of microRNAs in Obesity-Related Kidney Disease.International journal of molecular sciences · 2021
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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

11 authors at 5 institutions in 1 country.

Da SunInstitute of Life Sciences, Wenzhou University, Wenzhou, China.ORCID 0000-0001-7747-9951
Jia ChenSichuan Provincial Center for Mental Health, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, Chengdu, China.
Wei WuInstitute of Life Sciences, Wenzhou University, Wenzhou, China.
Ju TangMedical Research Center, Southwest Hospital Third Military Medical University, Chongqing, China.
Li LuoBioengineering College, Chongqing University, Chongqing, China.
Kun ZhangBioengineering College, Chongqing University, Chongqing, China.
Libo JinInstitute of Life Sciences, Wenzhou University, Wenzhou, China.
Sue LinInstitute of Life Sciences, Wenzhou University, Wenzhou, China.
Yitian GaoInstitute of Life Sciences, Wenzhou University, Wenzhou, China.
Xiaoqing YanSchool of Pharmaceutical Sciences at the Wenzhou Medical University, Wenzhou, China.
Chi ZhangThe Third Affiliated Hospital of Wenzhou Medical University, Ruian, Wenzhou, China.
Wenzhou University · CNChongqing University · CNWenzhou Medical University · CNArmy Medical University · CNSichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Obesity is associated with significant microvascular complications including renal injuries and may induce end-stage renal disease. Emerging studies have demonstrated microRNAs (miRNAs) are potential mediators in the pathophysiological process of nephropathy. The present study aimed to investigate the role of miR-802 in obesity-related nephropathy and potential molecular mechanisms. Through utilizing obese mouse model and human subjects, we explored the therapeutic benefits and clinical application of miR-802 in protecting against nephropathy. Renal miR-802 level was positively correlated with functional parameters, including blood urea nitrogen and creatinine in obese mice. Specific silencing of renal miR-802 improved high fat diet (HFD)-induced renal dysfunction, structural disorders and fibrosis. The up-regulated inflammatory response and infiltrated macrophages were also significantly decreased in miR-802 inhibitor-treated obese mice. Mechanistically, miR-802 directly bond to 3'-UTR of NF-κB-repressing factor (NRF) and suppressed its expression. In clinical study, the circulating miR-802 level was significantly increased in obese subjects, and positively correlated with plasma creatinine level but negatively correlated with creatinine clearance. Taken together, our findings provided evidence that miR-802/NRF signalling was an important pathway in mediating obesity-related nephropathy. It is a possible useful clinical approach of treating miR-802 inhibitor to combat nephropathy.

Indexed as

Disease Models, AnimalGene Expression RegulationAnimalsDiet, High-FatHumansKidney DiseasesMaleMiceMice, ObeseMicroRNAsNF-kappa BObesityRepressor ProteinsSignal TransductionMicroRNAsMIRN802 microRNA, humanMIRN802 microRNA, mouseNF-kappa BNKRF protein, humanRepressor ProteinsinflammationnephropathyNF-κB-repressing factorobesity

Identifiers

PMID30729676
PMCPMC6433720
OpenAlexW2913361768

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.