Evidence map›Paper›PMID 35867293›Full record

ArticleJournal of bioenergetics and biomembranes2022

The potential role of circulating exosomes in protecting myocardial injury in acute myocardial infarction via regulating miR-190a-3p/CXCR4/CXCL12 pathway.

Chun-Yuan Jiang, Ting-Ting Zhong, Lu-Wen Qiu, Yan-Feng Liu, Hui-Hua Zuo, Xiao-Fei Huang

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of bioenergetics and biomembranes, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

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  12. Endothelial progenitor cells in pregnancy-related diseases.Clinical science (London, England : 1979) · 2023
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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

6 authors at 2 institutions in 1 country.

Chun-Yuan Jiang *Department of Cardiology, Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College, Jiangxi, 330006, Nanchang, China.
Ting-Ting Zhong *Department of Cardiology, Fuwai Hospital, Chinese Academy of Medical Sciences, Shenzhen, (Shenzhen Sun Yat-Sen Cardiovascular Hospital), Shenzhen, 518057, China. zhongtt6@mail2.sysu.edu.cn.
Lu-Wen QiuDepartment of Cardiology, Fuwai Hospital, Chinese Academy of Medical Sciences, Shenzhen, (Shenzhen Sun Yat-Sen Cardiovascular Hospital), Shenzhen, 518057, China.
Yan-Feng LiuDepartment of Cardiology, Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College, Jiangxi, 330006, Nanchang, China.
Hui-Hua ZuoDepartment of Cardiology, Fuwai Hospital, Chinese Academy of Medical Sciences, Shenzhen, (Shenzhen Sun Yat-Sen Cardiovascular Hospital), Shenzhen, 518057, China.
Xiao-Fei HuangDepartment of Cardiology, Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College, Jiangxi, 330006, Nanchang, China.
Chinese Academy of Medical Sciences & Peking Union Medical College · CNJiangxi Provincial People's Hospital · CN

Funding

academician shengshou hu youth talent cultivation fund YS-2020-007shenzhen fundamental research program JCYJ20180703145002040
6 · The paper itself

Abstract

Exosomes of different origins have been found to be protective against ischemic-induced myocardial injury. This study examined the protective effects of circulating exosomes in the mice model of acute myocardial infarction (AMI) and explored the underlying molecular mechanisms. The effects of exosomes on myocardial injury were assessed in the AMI mice model. The in vivo studies showed that circulating exosomes reduced the infarcted size, improved the morphology of heart tissues and also reduced apoptosis of the heart tissues. In addition, the model mice showed an increase in the CD34 + /VEGFR2 + cell population and CD31, CXCR4 and CXCL12 expression after exosomes treatment. MiR-190a-3p was significantly down-regulated in the exosomes derived from the culture medium of hypoxia-treated human cardiomyocytes (HCMs). Further analysis revealed that miR-190a-3p could physically interact with CXCR4/CXCL12 by targeting the respective 3'UTRs. These exosomes could up-regulated CXCR4 and CXCL12 expression in the EPCs; in addition, miR-190a-3p mimics repressed CXCR4/CXCL12 expression in EPCs, while its inhibitor had opposite effects. The in vitro functional assays showed that miR-190a-3p overexpression suppressed the cell viability, proliferation, migration, adhesion and tube formation of EPCs; while miR-190a-3p inhibitor had the opposite effects; exosomes derived from the culture medium of hypoxia-treated HCMs exhibited similar actions of miR-190a-3p inhibitor. Moreover, miR-190a-3p was down-regulated in exosomes from serum in the AMI group when compared to that from sham group. Treatment with exosomes from serum in the AMI group promoted cell proliferation, migration, adhesion and tube formation of EPCs when compared to that in the sham group. More importantly, IT1t attenuated the enhanced effects of miR-190a-3p inhibition on EPC proliferation, migration, adhesion and tube formation. In conclusion, circulating exosomes exerted protective effects on myocardial injury in the AMI mice model, and down-regulation of miR-190a-3p in the circulating exosomes may exert protective effects against myocardial injury. Hypoxia induced the downregulation of miR-190a-3p in the culture medium of HCMs, and the mechanistic investigations indicated that exosomes of hypoxia-conditioned HCM culture medium promoted the cell viability, proliferation, migration, adhesion and tube formation of EPCs via regulating miR-190a-3p/CXCR4/CXCL12 pathway.

Indexed as

ExosomesMicroRNAsMyocardial Infarction3' Untranslated RegionsAnimalsApoptosisChemokine CXCL12HumansHypoxiaMiceReceptors, CXCR43' Untranslated RegionsChemokine CXCL12CXCL12 protein, humanCXCR4 protein, humanMicroRNAsReceptors, CXCR4Acute myocardial infarctionCXCL12CXCR4EPCsExosomesmiR-190a-3p

Identifiers

PMID35867293
OpenAlexW4286717489

What OpenQuestion holds

Textmetadata
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.