Evidence map›Paper›PMID 26330104›Full record

ArticleScientific reports2015

Effect of miR-34a in regulating steatosis by targeting PPARα expression in nonalcoholic fatty liver disease.

Jiexia Ding, Meng Li, Xingyong Wan, Xi Jin, Shaohua Chen, Chaohui Yu, Youming Li

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

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 162 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
162citing papers in PubMed, 4 pooled it
6.4field-weighted citation impact, top 2% 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

162 citing papers in PubMed, 4 syntheses or guidelines pooled it, 255 citations in OpenAlex.

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102 more citing papers are in PubMed but not listed here.

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

7 authors at 2 institutions in 1 country.

Jiexia DingDepartment of Infectious Diseases, Hangzhou First People's Hospital, No. 261 Huansha Road, Hangzhou 310006, Zhejiang Province, China.
Meng LiDepartment of Gastroenterology, The First Affiliated Hospital, Medical School, Zhejiang University, No. 79 Qingchun Road, Hangzhou 310003, Zhejiang Province, China.
Xingyong WanDepartment of Gastroenterology, The First Affiliated Hospital, Medical School, Zhejiang University, No. 79 Qingchun Road, Hangzhou 310003, Zhejiang Province, China.
Xi JinDepartment of Gastroenterology, The First Affiliated Hospital, Medical School, Zhejiang University, No. 79 Qingchun Road, Hangzhou 310003, Zhejiang Province, China.
Shaohua ChenDepartment of Gastroenterology, The First Affiliated Hospital, Medical School, Zhejiang University, No. 79 Qingchun Road, Hangzhou 310003, Zhejiang Province, China.
Chaohui YuDepartment of Gastroenterology, The First Affiliated Hospital, Medical School, Zhejiang University, No. 79 Qingchun Road, Hangzhou 310003, Zhejiang Province, China.
Youming LiDepartment of Gastroenterology, The First Affiliated Hospital, Medical School, Zhejiang University, No. 79 Qingchun Road, Hangzhou 310003, Zhejiang Province, China.
Zhejiang University · CNHangzhou First People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNA-34a (miR-34a) is thought to be involved in nonalcoholic fatty liver disease (NAFLD). However, the association between altered expression of miR-34a and the pathophysiological features of NAFLD remains unclear. Here, we investigated the mechanisms by which miR-34a influences NAFLD through the PPARα-related pathway. Real-time quantitative PCR, western blotting and other assays kit were used to investigate the expression and function of miR-34a in an NAFLD model. Cultured cells transfected with miR-34a inhibitor and C57BL/6 mice injected with the miR-34a inhibitor through vein tail were conducted for the effects of miR-34a on its target. MiR-34a levels were significantly upregulated in steatosis-induced hepatocytes and in liver tissues of high-fat diet-fed mice. The upregulation of miR-34a resulted in the downregulation of hepatic PPARα and SIRT1 that are the direct targets of miR-34a. Silencing miR-34a led to an initially increased expression of PPARα, SIRT1 and PPARα's downstream genes. Activation of the central metabolic sensor AMPK was also increased. The miR-34a inhibitor suppressed lipid accumulation and improved the degree of steatosis. Taken together, our data indicated that decreased expression of miR-34a potentially contributes to altered lipid metabolism in NAFLD. Downregulation of miR-34a may be a therapeutic strategy against NAFLD by regulating its target PPARα and SIRT1.

Indexed as

Adenylate KinaseAnimalsAspartate AminotransferasesBase SequenceCell LineDiet, High-FatFatty AcidsGene Expression ProfilingHumansLiverMaleMice, Inbred C57BLMicroRNAsMolecular Sequence DataNon-alcoholic Fatty Liver DiseasePhosphorylationAdenylate KinaseAspartate AminotransferasesFatty AcidsMicroRNAsMIRN34a microRNA, mouseMIRN34 microRNA, humanPPAR alphaSirtuin 1

Identifiers

PMID26330104
PMCPMC4557122
OpenAlexW2404854535

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.