Evidence map›Paper›PMID 32582976›Full record

ArticleInternational journal of molecular medicine2020

miR‑148a‑3p regulates alcoholic liver fibrosis through targeting ERBB3.

Jie Xiong, Jianbo Ni, Congying Chen, Kezhou Wang

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

21 citing papers in PubMed, 29 citations in OpenAlex.

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  13. Insights on drug and gene delivery systems in liver fibrosis.Asian journal of pharmaceutical sciences · 2023
    Review
  14. Article
  15. Article
  16. MicroRNA 148a Suppresses Tuberculous Fibrosis by Targeting NOX4 and POLDIP2.International journal of molecular sciences · 2022
    Article
  17. Article
  18. Review
  19. Review
  20. Article
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 XiongDepartment of Gastroenterology and Hepatology, Tongji Hospital, Tongji University School of Medicine, Shanghai 200065, P.R. China.
Jianbo NiDepartment of Gastroenterology and Hepatology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, P.R. China.
Congying ChenDepartment of Gastroenterology and Hepatology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, P.R. China.
Kezhou WangDepartment of Pathology, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200092, P.R. China.
Shanghai Jiao Tong University · CNTongji Hospital · CNXinHua Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alcoholic liver disease greatly affects human health. Previous studies have identified that microRNAs (miRNAs) are associated with the pathogenesis of alcoholic liver fibrosis (ALF). Therefore, the present study explored the regulatory mechanism of miR‑148a‑3p in ALF. An ALF model was established in rats by alcohol gavage, followed by treatment with miR‑148a‑3p. Reverse transcription‑quantitative (RT‑q) PCR was performed to detect miR‑148a‑3p expression in the rat liver tissues. The levels of lactate dehydrogenase (LDH), aspartate aminotransferase (AST), alanine transaminase (ALT) and alkaline phosphatase (ALP) were determined by enzyme‑labeled colorimetry. Liver damage was evaluated by liver indices and histology. The direct target gene of miR‑148a‑3p was predicted by a dual luciferase reporter assay. The effects of miR‑148a‑3p and miR‑148a‑3p in combination with receptor tyrosine‑protein kinase erbB‑3 (ERBB3) on HSC‑T6 cell viability and apoptosis were detected by MTT and flow cytometry assays, respectively. Western blotting and RT‑qPCR assays were performed to detect the expression levels of proteins and mRNA associated with fibrosis and apoptosis. The data showed that miR‑148a‑3p mimics inhibited the expression levels of AST, ALT, ALP, LDH, α‑SMA and type I collagen in the model, decreased the liver indices, and improved the liver damage caused by alcohol. ERBB3, which was predicted as the direct target gene of miR‑148a‑3p, reversed the effects of ERBB3 on promoting cell viability and inhibiting apoptosis. Concomitantly, miR‑148a‑3p reversed the increased expression of Bcl‑2 and inhibited the expression levels of Bax and c‑cleaved‑3 caused by ERBB3. These data suggested that miR‑148a‑3p regulated ALF and the viability and apoptosis of hepatic stellate cells through targeting ERBB3.

Indexed as

Alanine TransaminaseAnimalsApoptosisAspartate AminotransferasesCell SurvivalHepatic Stellate CellsLiverLiver CirrhosisLiver Diseases, AlcoholicL-Lactate DehydrogenaseMaleMicroRNAsRatsReceptor, ErbB-3Alanine TransaminaseAspartate AminotransferasesErbb3 protein, ratL-Lactate DehydrogenaseMicroRNAsReceptor, ErbB-3

Identifiers

PMID32582976
PMCPMC7387083
OpenAlexW3035846566

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.