Evidence map›Paper›PMID 32070295›Full record

ArticleBMC gastroenterology2020

Uric acid induced hepatocytes lipid accumulation through regulation of miR-149-5p/FGF21 axis.

Shenghui Chen, Dan Chen, Hua Yang, Xinyu Wang, Jinghua Wang, Chengfu Xu

Open access · goldAbstract read
In one paragraph

Article in BMC gastroenterology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
4.9field-weighted citation impact, top 4% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 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 2 institutions in 1 country.

Shenghui ChenDepartment of Gastroenterology, the First Affiliated Hospital, College of Medicine, Zhejiang University, 79 Qingchun Road, Hangzhou, 310003, Zhejiang Province, China.
Dan ChenDepartment of Gastroenterology, the First Affiliated Hospital, College of Medicine, Zhejiang University, 79 Qingchun Road, Hangzhou, 310003, Zhejiang Province, China.
Hua YangDepartment of Gastroenterology, the First Affiliated Hospital, College of Medicine, Zhejiang University, 79 Qingchun Road, Hangzhou, 310003, Zhejiang Province, China.
Xinyu WangDepartment of Gastroenterology, the First Affiliated Hospital, College of Medicine, Zhejiang University, 79 Qingchun Road, Hangzhou, 310003, Zhejiang Province, China.
Jinghua WangDepartment of Gastroenterology, the First Affiliated Hospital, College of Medicine, Zhejiang University, 79 Qingchun Road, Hangzhou, 310003, Zhejiang Province, China.
Chengfu XuDepartment of Gastroenterology, the First Affiliated Hospital, College of Medicine, Zhejiang University, 79 Qingchun Road, Hangzhou, 310003, Zhejiang Province, China. xiaofu@zju.edu.cn.ORCID http://orcid.org/0000-0002-6172-1253
Zhejiang University · CNFirst Affiliated Hospital Zhejiang University · CN

Funding

Fundamental Research Funds for the Central Universities 2018XZZX002-10Fundamental Research Funds for the Central Universities 2019QNA7034Key Research and Development Program of Zhejiang Province 2020C03033National Natural Science Foundation of China 81722009,National Natural Science Foundation of China 81770573National Natural Science Foundation of China 81870400
6 · The paper itself

Abstract

backgroundHyperuricemia is a major risk for non-alcoholic fatty liver disease. However, the mechanisms for this phenomenon are not fully understood. This study aimed to investigate whether microRNAs mediated the pathogenic effects of uric acid on non-alcoholic fatty liver disease.

methodsMicroarray was used to determine the hepatic miRNA expression profiles of male C57BL/6 mice fed on standard chow diet, high fat diet (HFD), and HFD combined with uric acid-lowering therapy by allopurinol. We validated the expression of the most significant differentially expressed microRNAs and explored its role and downstream target in uric acid-induced hepatocytes lipid accumulation.

resultsMicroarray analysis and subsequent validation showed that miR-149-5p was significantly up-regulated in the livers of HFD-fed mice, while the expression was down-regulated by allopurinol therapy. MiR-149-5p expression was also significantly up-regulated in uric acid-stimulated hepatocytes. Over-expression of miR-149-5p significantly aggregated uric acid-induced triglyceride accumulation in hepatocytes, while inhibiting miR-149-5p ameliorated the triglyceride accumulation. Luciferase report assay confirmed that FGF21 is a target gene of miR-149-5p. Silencing FGF21 abolished the ameliorative effects of miR-149-5p inhibitor on uric acid-induced hepatocytes lipid accumulation, while overexpression of FGF21 prevented the lipid accumulation induced by miR-149-5p mimics.

conclusionsUric acid significantly up-regulated the expression of miR-149-5p in hepatocytes and induced hepatocytes lipid accumulation via regulation of miR-149-5p/FGF21 axis.

Indexed as

AllopurinolAnimalsAntimetabolitesDiet, High-FatEnzyme InhibitorsFibroblast Growth FactorsHepatocytesHyperuricemiaMaleMiceMice, Inbred C57BLMicroRNAsNon-alcoholic Fatty Liver DiseaseTriglyceridesUp-RegulationUric AcidAllopurinolAntimetabolitesEnzyme Inhibitorsfibroblast growth factor 21Fibroblast Growth FactorsMicroRNAsMIRN149 microRNA, humanTriglyceridesUric AcidXanthine OxidasemiR-149-5pNon-alcoholic fatty liver diseaseUric acid

Identifiers

PMID32070295
PMCPMC7027271
OpenAlexW3012420683

What OpenQuestion holds

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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 OpenQuestion graph.