Evidence map›Paper›PMID 32648079›Full record

ArticleDigestive diseases and sciences2021

MicroRNA-503 Targets Mothers Against Decapentaplegic Homolog 7 Enhancing Hepatic Stellate Cell Activation and Hepatic Fibrosis.

Xia Xie, Cheng-Yun Dou, Yu Zhou, Quan Zhou, Hai-Bo Tang

Abstract read
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In one paragraph

Article in Digestive diseases and sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

11 citing papers in PubMed, 19 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

5 authors at 2 institutions in 1 country.

Xia XieDepartment of Infectious Diseases, The First Affiliated Hospital of University of South China, Hengyang, 421001, Hunan, China.
Cheng-Yun DouDepartment of Infectious Diseases, The First Affiliated Hospital of University of South China, Hengyang, 421001, Hunan, China.
Yu ZhouDepartment of Pathology, The Second Affiliated Hospital of University of South China, Hengyang, 421001, China.
Quan ZhouDepartment of Infectious Diseases, The First Affiliated Hospital of University of South China, Hengyang, 421001, Hunan, China.
Hai-Bo TangDepartment of Infectious Diseases, The First Affiliated Hospital of University of South China, Hengyang, 421001, Hunan, China. 252286374@qq.com.ORCID http://orcid.org/0000-0002-0448-4503
First Affiliated Hospital of University of South China · CNUniversity of South China · CN

Funding

the Guiding Projects of Hengyang City, 2018 S2018F9031021273
6 · The paper itself

Abstract

backgroundThe hyper-accumulation of extracellular matrix (ECM) is the leading cause of hepatic fibrosis, and TGF-β-induced activation of hepatic stellate cells (HSCs) is the central event of hepatic fibrosis pathogenesis. The deregulation and dysfunction of miRNAs in hepatic fibrosis have been reported previously.

aimsTo identify miRNA(s) playing a role in HSC activation and the underlying mechanism.

methodsWe analyzed online microarray expression datasets from Gene Expression Omnibus (GEO) for differentially expressed miRNAs in hepatic fibrosis-related disease liver tissues, examined the specific effects of the candidate miRNA on TGF-β-induced HSC activation, and screened for the targets of the candidate miRNA in the TGF-β/SMAD signaling. Then, the predicted miRNA-mRNA binding, the specific effects of the target mRNA, and the dynamic effects of miRNA and mRNA on TGF-β-induced HSC activation were investigated.

resultsThe miR-503 expression was upregulated in TGF-β-activated HSCs. miR-503 overexpression enhanced, while miR-503 inhibition attenuated TGF-β-induced HSC proliferation and ECM accumulation in HSCs. miR-503 targeted SMAD7 to inhibit SMAD7 expression. SMAD7 knockdown also aggravated TGF-β-induced HSC proliferation and ECM accumulation in HSCs. The effects of miR-503 overexpression on TGF-β-induced HSC activation were partially reversed by SMAD7 overexpression. In CCl

conclusionmiR-503 acts on HSC activation and hepatic fibrosis through SMAD7. The miR-503/SMAD7 axis enhances HSC activation and hepatic fibrosis through the TGF-β/SMAD pathway.

Indexed as

AnimalsCarbon TetrachlorideHepatic Stellate CellsHumansLiver CirrhosisMicroRNAsRatsRats, Sprague-DawleySmad7 ProteinCarbon TetrachlorideMicroRNAsMIRN503 microRNA, humanSmad7 ProteinSMAD7 protein, humanExtracellular matrix (ECM)Hepatic fibrosisHepatic stellate cells (HSCs)miR-503SMAD7TGF-β

Identifiers

PMID32648079
OpenAlexW3041116466

What OpenQuestion holds

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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.