Evidence map›Paper›PMID 33881681›Full record

ArticleInflammation2021

Adipose-Derived Mesenchymal Stem Cells-Derived Exosomes Carry MicroRNA-671 to Alleviate Myocardial Infarction Through Inactivating the TGFBR2/Smad2 Axis.

Xue Wang, Yuhai Zhu, Chengcheng Wu, Wennan Liu, Yujie He, Qing Yang

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Inflammation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 1 pooled it
4.8field-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

62 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.

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2 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

6 authors at 2 institutions in 1 country.

Xue Wang *Department of Cardiology, Tianjin Medical University General Hospital, NO. 154, Anshan Street, Heping District, Tianjin, 300052, People's Republic of China.
Yuhai Zhu *Department of Medical Cosmetology, Tianjin Medical University General Hospital Airport Hospital, Tianjin, 300308, People's Republic of China.
Chengcheng WuDepartment of Cardiology, Tianjin Medical University General Hospital, NO. 154, Anshan Street, Heping District, Tianjin, 300052, People's Republic of China.
Wennan LiuDepartment of Cardiology, Tianjin Medical University General Hospital, NO. 154, Anshan Street, Heping District, Tianjin, 300052, People's Republic of China.
Yujie HeDepartment of Cardiology, Tianjin Beichen District Chinese Medicine Hospital, Tianjin, 300400, People's Republic of China.
Qing YangDepartment of Cardiology, Tianjin Medical University General Hospital, NO. 154, Anshan Street, Heping District, Tianjin, 300052, People's Republic of China. Yangqing9911@163.com.ORCID http://orcid.org/0000-0002-2048-4087
Tianjin Medical University General Hospital · CNTianjin Beichen Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mesenchymal stem cells (MSCs) and their derived extracellular vesicles have been reported as promising tools for the management of heart disease. The aim of this study was to explore the function of adipose-derived MSCs (adMSCs)-derived exosomes (Exo) in the progression of myocardial infarction (MI) and the molecules involved. Mouse cardiomyocytes were treated with oxygen-glucose deprivation (OGD) to mimic an MI condition in vitro. The adMSCs-derived Exo were identified and administrated into the OGD-treated cardiomyocytes, and then the viability and apoptosis of cells, and the secretion of fibrosis- and inflammation-related cytokines in cells were determined. Differentially expressed microRNAs (miRNAs) in cells after Exo treatment were screened using a microarray analysis. The downstream molecules regulated by miR-671 were explored through bioinformatic analysis. Involvements of miR-671 and transforming growth factor beta receptor 2 (TGFBR2) in the exosome-mediated events were confirmed by rescue experiments. A murine model with MI was induced and treated with Exo for functional experiments in vivo. Compared to phosphate-buffered saline treatment, the Exo treatment significantly enhanced viability while reduced apoptosis of cardiomyocytes, and in reduced myocardial fibrosis and inflammation both in vitro and in vivo. miR-671 was significantly upregulated in cells after Exo treatment. Downregulation of miR-671 blocked the protective functions of Exo. miR-671 targeted TGFBR2 and suppressed phosphorylation of Smad2. Artificial downregulation of TGFBR2 enhanced viability of the OGD-treated cardiomyocytes. This study suggested that adMSC-derived exosomal miR-671 directly targets TGFBR2 and reduces Smad2 phosphorylation to alleviate MI-like symptoms both in vivo and in vitro.

Indexed as

AnimalsCell HypoxiaCells, CulturedExosomesGlucoseMesenchymal Stem CellsMesenchymal Stem Cell TransplantationMiceMice, Inbred C57BLMice, TransgenicMicroRNAsMyocardial InfarctionMyocytes, CardiacReceptor, Transforming Growth Factor-beta Type IISmad2 ProteinGlucoseMicroRNAsMIRN671 microRNA, mouseReceptor, Transforming Growth Factor-beta Type IISmad2 ProteinSmad2 protein, mouseTgfbr2 protein, mouseexosomesmicroRNA-671MSCmyocardial infarctionSmad2TGFBR2

Identifiers

PMID33881681
PMCPMC8460592
OpenAlexW3156541535

What OpenQuestion holds

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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.