Evidence map›Paper›PMID 39009669›Full record

ArticleScientific reports2024

EVs-miR-17-5p attenuates the osteogenic differentiation of vascular smooth muscle cells potentially via inhibition of TGF-β signaling under high glucose conditions.

Isashi Baba, Tetsuya Matoba, Shunsuke Katsuki, Jun-Ichiro Koga, Takuro Kawahara, Mitsukuni Kimura, Hidetaka Akita, Hiroyuki Tsutsui

Erratum issuedAbstract read
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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

15 citing papers in PubMed.

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  10. Considerations on the Development of Therapeutics in Vascular Calcification.Journal of cardiovascular development and disease · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors.

Isashi BabaDepartment of Cardiovascular Medicine, Graduate School of Medical Sciences, Kyushu University, 3-1-1, Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan.
Tetsuya MatobaDepartment of Cardiovascular Medicine, Graduate School of Medical Sciences, Kyushu University, 3-1-1, Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan. matoba@cardiol.med.kyushu-u.ac.jp.
Shunsuke KatsukiDepartment of Cardiovascular Medicine, Graduate School of Medical Sciences, Kyushu University, 3-1-1, Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan.
Jun-Ichiro KogaSecond Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan.
Takuro KawaharaDepartment of Cardiovascular Medicine, Graduate School of Medical Sciences, Kyushu University, 3-1-1, Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan.
Mitsukuni KimuraDepartment of Cardiovascular Medicine, Graduate School of Medical Sciences, Kyushu University, 3-1-1, Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan.
Hidetaka AkitaLaboratory of Drug Design and Drug Disposition, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai, Japan.
Hiroyuki TsutsuiDepartment of Cardiovascular Medicine, Graduate School of Medical Sciences, Kyushu University, 3-1-1, Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan.

Funding

CREST JPMJCR17H5JSPS KAKENHI JP21H02916
6 · The paper itself

Abstract

Vascular calcification, which is a major complication of diabetes mellitus, is an independent risk factor for cardiovascular disease. Osteogenic differentiation of vascular smooth muscle cells (VSMCs) is one of the key mechanisms underlying vascular calcification. Emerging evidence suggests that macrophage-derived extracellular vesicles (EVs) may be involved in calcification within atherosclerotic plaques in patients with diabetes mellitus. However, the role of macrophage-derived EVs in the progression of vascular calcification is largely unknown. In this study, we investigated whether macrophage-derived EVs contribute to the osteogenic differentiation of VSMCs under high glucose conditions. We isolated EVs that were secreted by murine peritoneal macrophages under normal glucose (EVs-NG) or high glucose (EVs-HG) conditions. miRNA array analysis in EVs from murine macrophages showed that miR-17-5p was significantly increased in EVs-HG compared with EVs-NG. Prediction analysis with miRbase identified transforming growth factor β receptor type II (TGF-β RII) as a potential target of miR-17-5p. EVs-HG as well as miR-17-5p overexpression with lipid nanoparticles inhibited the gene expression of Runx2, and TGF-β RII. Furthermore, we demonstrated that VSMCs transfected with miR-17-5p mimic inhibited calcium deposition. Our findings reveal a novel role of macrophage-derived EVs in the negative regulation of osteogenic differentiation in VSMCs under high glucose conditions.

Indexed as

Cell DifferentiationExtracellular VesiclesGlucoseMicroRNAsMuscle, Smooth, VascularMyocytes, Smooth MuscleOsteogenesisSignal TransductionTransforming Growth Factor betaAnimalsCore Binding Factor Alpha 1 SubunitMaleMiceMice, Inbred C57BLReceptor, Transforming Growth Factor-beta Type IIVascular CalcificationCore Binding Factor Alpha 1 SubunitGlucoseMicroRNAsMirn17 microRNA, mouseReceptor, Transforming Growth Factor-beta Type IITgfbr2 protein, mouseTransforming Growth Factor beta

Identifiers

PMID39009669
PMCPMC11251274

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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.