Evidence map›Paper›PMID 32040481›Full record

ArticlePloS one2020

The association between microRNA-21 and hypertension-induced cardiac remodeling.

Ken Watanabe, Taro Narumi, Tetsu Watanabe, Yoichiro Otaki, Tetsuya Takahashi, Tomonori Aono, Jun Goto, Taku Toshima, Takayuki Sugai, Masahiro Wanezaki and 8 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.5field-weighted citation impact, top 3% 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

38 citing papers in PubMed, 79 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

18 authors at 2 institutions in 1 country.

Ken WatanabeDepartment of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan.ORCID 0000-0001-8499-8717
Taro NarumiDepartment of Cardiology, Internal Medicine III, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Tetsu WatanabeDepartment of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan.
Yoichiro OtakiDepartment of Advanced Cardiovascular Therapeutics, Yamagata University School of Medicine, Yamagata, Japan.
Tetsuya TakahashiDepartment of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan.
Tomonori AonoDepartment of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan.
Jun GotoDepartment of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan.
Taku ToshimaDepartment of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan.
Takayuki SugaiDepartment of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan.
Masahiro WanezakiDepartment of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan.
Daisuke KutsuzawaDepartment of Advanced Heart Rhythm Therapeutics, Yamagata University School of Medicine, Yamagata, Japan.
Shigehiko KatoDepartment of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan.
Harutoshi TamuraDepartment of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan.
Satoshi NishiyamaDepartment of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan.
Hiroki TakahashiDepartment of Advanced Cardiovascular Therapeutics, Yamagata University School of Medicine, Yamagata, Japan.
Takanori ArimotoDepartment of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan.
Tetsuro ShishidoDepartment of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan.
Masafumi WatanabeDepartment of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan.
Yamagata University · JPHamamatsu University School of Medicine · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypertension is a major public health problem among the aging population worldwide. It causes cardiac remodeling, including hypertrophy and interstitial fibrosis, which leads to development of hypertensive heart disease (HHD). Although microRNA-21 (miR-21) is associated with fibrogenesis in multiple organs, its contribution to cardiac remodeling in hypertension is poorly understood. Circulating miR-21 level was higher in patients with HHD than that in the control subjects. It also positively correlated with serum myocardial fibrotic markers. MiR-21 expression levels were significantly upregulated in the mice hearts after angiotensin II (Ang II) infusion or transverse aortic constriction (TAC) compared with control mice. Expression level of programmed cell death 4 (PDCD4), a main target of miR-21, was significantly decreased in Ang II infused mice and TAC mice compared with control mice. Expression levels of transcriptional activator protein 1 (AP-1) and transforming growth factor-β1 (TGF-β1), which were downstream targets of PDCD4, were increased in Ang II infused mice and TAC mice compared with control mice. In vitro, mirVana-miR-21-specific inhibitor attenuated Ang II-induced PDCD4 downregulation and contributed to subsequent deactivation of AP-1/TGF-β1 signaling pathway in neonatal rat cardiomyocytes. Thus, suppression of miR-21 prevents hypertrophic stimulation-induced cardiac remodeling by regulating PDCD4, AP-1, and TGF-β1 signaling pathway.

Indexed as

AgedAngiotensin IIAnimalsAnimals, NewbornApoptosis Regulatory ProteinsCardiomegalyDisease Models, AnimalFemaleFibrosisHumansHypertensionMaleMiceMice, Inbred C57BLMicroRNAsMiddle AgedAngiotensin IIApoptosis Regulatory ProteinsMicroRNAsMIRN21 microRNA, humanMIRN21 microRNA, mousemirn21 microRNA, ratPdcd4 protein, mousePdcd4 protein, ratRNA-Binding ProteinsTgfb1 protein, mouseTgfb1 protein, ratTranscription Factor AP-1Transforming Growth Factor beta1

Identifiers

PMID32040481
PMCPMC7010249
OpenAlexW3006257674

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.