Evidence map›Paper›PMID 35188624›Full record

ArticleHepatology international2022

miR-98-5p as a novel biomarker suppress liver fibrosis by targeting TGFβ receptor 1.

Yanhua Ma, Xiaoxue Yuan, Ming Han, Yifan Xu, Kai Han, Pu Liang, Shunai Liu, Jun Chen, Huichun Xing

Abstract read
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In one paragraph

Article in Hepatology international, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

8 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Article
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  6. Article
  7. Role of noncoding RNAs in liver fibrosis.World journal of gastroenterology · 2023
    Review
  8. Review
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

9 authors at 2 institutions in 1 country.

Yanhua Ma *Peking University Ditan Teaching Hospital, Peking University Health Science Center, Beijing, China.
Xiaoxue Yuan *Beijing Key Laboratory of Emerging Infectious Diseases, Beijing, China.ORCID http://orcid.org/0000-0002-2886-4703
Ming HanBeijing Key Laboratory of Emerging Infectious Diseases, Beijing, China.
Yifan XuPeking University Ditan Teaching Hospital, Peking University Health Science Center, Beijing, China.
Kai HanBeijing Key Laboratory of Emerging Infectious Diseases, Beijing, China.
Pu LiangBeijing Key Laboratory of Emerging Infectious Diseases, Beijing, China.
Shunai LiuBeijing Key Laboratory of Emerging Infectious Diseases, Beijing, China.
Jun ChenPeking University Ditan Teaching Hospital, Peking University Health Science Center, Beijing, China. chengj0817@sina.cn.
Huichun XingPeking University Ditan Teaching Hospital, Peking University Health Science Center, Beijing, China. hchxing@sohu.com.ORCID http://orcid.org/0000-0002-9111-9669
Capital Medical University · CNBinzhou Medical University · CN

Funding

beijing nova program Z201100006820051national major science and technology projects of china 2014ZX10005001
6 · The paper itself

Abstract

backgroundHepatic fibrosis is the repair reaction of excessive deposition and abnormal distribution of extracellular matrix after various liver injuries, especially chronic HBV infection, which is a key step in the development of various chronic liver diseases to cirrhosis. Recent studies have showed that microRNAs (miRNAs) can regulate a series of liver fibrosis-related gene express and play an important role in the development of liver fibrosis. But the miRNAs expression profiling and the differentially expressed miRNAs in patients with HBV-related liver fibrosis were little known. This study aims to have a record of a systemic screening for liver fibrosis-associated miRNAs in patients infected with HBV.

methodsA IlluminaHiSeq sequencing of plasma miRNAs from the HBV-related liver fibrosis patients (S2/3, n = 8) based on Scheuer's staging criteria and from healthy volunteers 42 (n = 7) was performed. Cluster analysis and target gene prediction were performed for the differentially expressed miRNAs. Gene ontology (GO) analysis and KEGG pathway enrichment analysis also were performed on the differentially expressed target miRNA genes.

resultsCompared with the healthy control group, 77 miRNAs were screened out from the liver fibrosis group, among which 51 miRNAs were up-regulated and 26 miRNAs were down-regulated. Eventually, miR-98-5p was identified as a candidate predictor of liver fibrosis progression. miR-98-5p is reduced in activated LX2 cells, and miR-98-5p overexpression inhibited the HSCs activation. Mechanically, MiR-98-5p prevents liver fibrosis by targeting TGFbR1 and blocking TGFb1/Smad3 signaling pathway. Furthermore, serum miR-98-5p levels were measured from a total of 70 recruited patients with chronic HBV infection and 29 healthy individuals as controls. Serum miR-98-5p level was significantly lower in patients with liver fibrosis than in healthy controls and HBV carriers.

conclusionsThe expression of miRNAs in patients with liver fibrosis is significantly different from that of healthy volunteers. Many signal pathways of hepatic fibrosis are regulated by miRNAs. The potential value of miR-98-5p is as diagnostic biomarkers and therapeutic targets for HBV-related liver fibrosis.

Indexed as

Liver CirrhosisMicroRNAsReceptor, Transforming Growth Factor-beta Type IBiomarkersCase-Control StudiesGene Expression ProfilingHumansSignal TransductionBiomarkersMicroRNAsMIRN98 microRNA, humanReceptor, Transforming Growth Factor-beta Type ITGFBR1 protein, humanBioinformatic analysisBiomarkerDifferential expressionHBV infectionLiver fibrosismiR-98-5pmiRNAsSignaling pathwayTarget genesTGFβR1

Identifiers

PMID35188624
OpenAlexW4225655962

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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.