Evidence map›Paper›PMID 29869625›Full record

ArticleExperimental & molecular medicine2018

MicroRNA-708-3p as a potential therapeutic target via the ADAM17-GATA/STAT3 axis in idiopathic pulmonary fibrosis.

Bo Liu, Rongrong Li, Jinjin Zhang, Chao Meng, Jie Zhang, Xiaodong Song, Changjun Lv

Open access · goldAbstract read
In one paragraph

Article in Experimental & molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
5.1field-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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 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

7 authors at 2 institutions in 1 country.

Bo LiuDepartment of Respiratory Medicine, Affiliated Hospital to Binzhou Medical University, Binzhou, China.
Rongrong LiDepartment of Respiratory Medicine, Affiliated Hospital to Binzhou Medical University, Binzhou, China.
Jinjin ZhangDepartment of Cellular and Genetic Medicine, School of Pharmaceutical Sciences, Binzhou Medical University, Yantai, China.
Chao MengDepartment of Respiratory Medicine, Affiliated Hospital to Binzhou Medical University, Binzhou, China.
Jie ZhangDepartment of Cellular and Genetic Medicine, School of Pharmaceutical Sciences, Binzhou Medical University, Yantai, China.
Xiaodong SongDepartment of Cellular and Genetic Medicine, School of Pharmaceutical Sciences, Binzhou Medical University, Yantai, China.
Changjun LvDepartment of Respiratory Medicine, Affiliated Hospital to Binzhou Medical University, Binzhou, China.
Binzhou University · CNBinzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs (miRNAs) are important diagnostic markers and therapeutic targets for many diseases. However, the miRNAs that control the pathogenesis of idiopathic pulmonary fibrosis (IPF) and act as potential therapeutic targets for the disease are rarely studied. In the present study, we analyzed the function and regulatory mechanism of microRNA-708-3p (miR-708-3p) and evaluated this marker's potential as a therapeutic target in IPF. The clinical and biological relevance of fibrogenesis for miR-708-3p was assessed in vivo and in vitro, specifically in matching plasma and tissue samples from 78 patients with IPF. The data showed that the miR-708-3p levels decreased during fibrosis and inversely correlated with IPF. The experiments showed that the decreased miR-708 promoter activity and primer-miR-708(pri-miR-708) expression were the potential causes. By computational analysis, a dual luciferase reporter system, rescue experiments and a Cignal Finder 45-Pathway system with siADAM17 and a miR-708-3p mimic, we identified that miR-708-3p directly regulates its target gene, a disintegrin and metalloproteinase 17 (ADAM17), through a binding site in the 3' untranslated region, which depends on the GATA/STAT3 signaling pathway. Finally, an miR-708-3p agomir was designed and used to test the therapeutic effects of the miR-708-3p in an animal model. Small-animal imaging technology and other experiments showed that the dynamic image distribution of the miR-708-3p agomir was mainly concentrated in the lungs and could block fibrogenesis. In conclusion, the miR-708-3p-ADAM17 axis aggravates IPF, and miR-708-3p can serve as a potential therapeutic target for IPF.

Indexed as

3' Untranslated RegionsA549 CellsADAM17 ProteinAgedAnimalsBlotting, WesternCell LineFemaleGATA Transcription FactorsHumansIdiopathic Pulmonary FibrosisMaleMicroRNAsMicroscopy, Electron, TransmissionMiddle AgedReal-Time Polymerase Chain Reaction3' Untranslated RegionsADAM17 ProteinADAM17 protein, humanGATA Transcription FactorsMicroRNAsMIRN708 microRNA, humanSTAT3 Transcription Factor

Identifiers

PMID29869625
PMCPMC5898903
OpenAlexW2795097509

What OpenQuestion holds

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LicenceCC BY
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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.