Evidence map›Paper›PMID 26637809›Full record

ArticleOncotarget2016

MicroRNA-17-5p-activated Wnt/β-catenin pathway contributes to the progression of liver fibrosis.

Fujun Yu, Zhongqiu Lu, Kate Huang, Xiaodong Wang, Ziqiang Xu, Bicheng Chen, Peihong Dong, Jianjian Zheng

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
4.6field-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

45 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.

  1. Pooled it
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  10. Hepatoprotective effects of diosmin: a narrative review.Naunyn-Schmiedeberg's archives of pharmacology · 2025
    Review
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  12. Frontiers in pharmacology · 2024
    Review
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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

8 authors at 2 institutions in 1 country.

Fujun YuDepartment of Infectious Diseases, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Zhongqiu LuEmergency Department, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Kate HuangDepartment of Pathology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Xiaodong WangDepartment of Infectious Diseases, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Ziqiang XuInstitute of Organ Transplantation, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Bicheng ChenKey Laboratory of Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Peihong DongDepartment of Infectious Diseases, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Jianjian ZhengKey Laboratory of Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Wenzhou Medical University · CNFirst Affiliated Hospital of Wenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aberrant Wnt/β-catenin pathway contributes to the development of liver fibrosis. MicroRNAs (MiRNAs) are found to act as regulators of the activation of hepatic stellate cell (HSC) in liver fibrosis. However, whether miRNAs activate Wnt/β-catenin pathway in activated HSCs during liver fibrosis is largely unknown. In this study, we found that Salvianolic acid B (Sal B) treatment significantly inhibited liver fibrosis in CCl4-treated rats, HSC-T6 cells and rat primary HSCs, resulting in the suppression of type I… collagen and alpha-smooth muscle actin. Also, Sal B suppressed HSC activation and cell proliferation in vitro. Interestingly, Sal B treatment induced the inactivation of Wnt/β-catenin pathway, with an increase in P-β-catenin and Wnt inhibitory factor 1 (WIF1). We demonstrated that the anti-fibrotic effects caused by Sal B were, at least in part, via WIF1. Moreover, our study revealed that miR-17-5p was reduced in vivo and in vitro after Sal B treatment. As confirmed by luciferase activity assays, WIF1 was a direct target of miR-17-5p. Notably, the suppression of HSCs induced by Sal B was almost inhibited by miR-17-5p mimics. Collectively, we demonstrated that miR-17-5p activates Wnt/β-catenin pathway to result in HSC activation through inhibiting WIF1 expression.

Indexed as

Gene Expression Regulation3' Untranslated RegionsAnimalsBenzofuransBlotting, WesternCarbon TetrachlorideCell LineCells, CulturedDepsidesDisease ProgressionDrugs, Chinese HerbalExtracellular Matrix ProteinsHepatic Stellate CellsImmunohistochemistryIntercellular Signaling Peptides and ProteinsLiver Cirrhosis3' Untranslated RegionsBenzofuransCarbon TetrachlorideDepsidesDrugs, Chinese HerbalExtracellular Matrix ProteinsIntercellular Signaling Peptides and ProteinsMicroRNAsMIRN17 microRNA, ratsalvianolic acid BWif1 protein, rathepatic stellate cellsmicroRNA-17-5pPathology SectionSalvianolic acid BWnt inhibitory factor 1 (WIF1)Wnt/β-catenin pathway

Identifiers

PMID26637809
PMCPMC4807984
OpenAlexW2283306839

What OpenQuestion holds

Textmetadata
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.