Evidence map›Paper›PMID 30894138›Full record

ArticleMolecular medicine (Cambridge, Mass.)2019

LncRNA PVT1 regulates atrial fibrosis via miR-128-3p-SP1-TGF-β1-Smad axis in atrial fibrillation.

Feng Cao, Zhe Li, Wen-Mao Ding, Ling Yan, Qing-Yan Zhao

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed
6.9field-weighted citation impact, top 2% 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

85 citing papers in PubMed, 132 citations in OpenAlex.

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25 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Feng CaoDepartment of Cardiology, Renmin Hospital of Wuhan University, NO.99 Zhangzhidong Road, Wuchang District, Wuhan, 430060, China. caofeng018@sina.com.
Zhe LiDepartment of Cardiology, Renmin Hospital of Wuhan University, NO.99 Zhangzhidong Road, Wuchang District, Wuhan, 430060, China.
Wen-Mao DingDepartment of Cardiology, Renmin Hospital of Wuhan University, NO.99 Zhangzhidong Road, Wuchang District, Wuhan, 430060, China.
Ling YanDepartment of Cardiology, Renmin Hospital of Wuhan University, NO.99 Zhangzhidong Road, Wuchang District, Wuhan, 430060, China.
Qing-Yan ZhaoDepartment of Cardiology, Renmin Hospital of Wuhan University, NO.99 Zhangzhidong Road, Wuchang District, Wuhan, 430060, China.
Renmin Hospital of Wuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLong non-coding RNAs (lncRNA) plasmacytoma variant translocation 1 (PVT1) has been shown to be associated with liver fibrosis. Nevertheless, the role of PVT1 in atrial fibrosis remains undefined. This study aims to elucidate the pathophysiological role of lncRNA PVT1 in the regulation of atrial fibrosis and to explore the underlying mechanism.

methodsExpression of PVT1, miR-128-sp, and Sp1 were examined in human atrial muscle tissues and angiotensin-II (Ang-II)-induced human atrial fibroblasts. Furthermore, the role of PVT1 in regulating atrial fibrosis in Ang-II-treated human atrial fibroblasts and Ang-II-induced atrial fibrosis in mice was investigated. Moreover, the interaction among PVT1, miR-128-3p, and Sp1 were examined using bioinformatics, expression correlation analysis, gain- or loss-of-function assays, RIP assays, and luciferase reporter assays. The involvement of transforming growth factor beta 1 (TGF-β1)/Smad pathway in this process was also explored.

resultsPVT1 was increased in atrial muscle tissues from AF patients and positively with collagen I and collagen III. In vitro assay revealed that PVT1 overexpression facilitated the Ang-II-induced atrial fibroblasts proliferation, collagen production, and TGF-β1/Smad signaling activation, whereas PVT1 knockdown caused the opposite effect. In vivo assay further confirmed that PVT1 knockdown attenuated the Ang-II-induced mouse atrial fibrosis. Mechanically, PVT1 acted as a sponge for miR-128-3p to facilitate Sp1 expression, thereby activating the TGF-β1/Smad signaling pathway.

conclusionLncRNA PVT1 promotes atrial fibrosis via miR-128-3p-SP1-TGF-β1-Smad axis in atrial fibrillation.

Indexed as

Atrial FibrillationAdultAngiotensin IIAnimalsCell ProliferationCollagen Type ICollagen Type IIFemaleFibroblastsFibrosisHeart AtriaHumansMaleMice, Inbred C57BLMicroRNAsMiddle AgedAngiotensin IICollagen Type ICollagen Type IIMicroRNAsMIRN128 microRNA, humanPVT1 long-non-coding RNA, humanRNA, Long NoncodingSmad ProteinsSP1 protein, humanSp1 Transcription FactorTGFB1 protein, humanTransforming Growth Factor beta1Atrial fibrillationAtrial fibrosismiR-128-3pPVT1Sp1TGF-β1/Smad signaling

Identifiers

PMID30894138
PMCPMC6425687
OpenAlexW2940070563

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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.