Evidence map›Paper›PMID 30814518›Full record

ArticleNature communications2019

Circulating myocardial microRNAs from infarcted hearts are carried in exosomes and mobilise bone marrow progenitor cells.

Min Cheng, Junjie Yang, Xiaoqi Zhao, Eric Zhang, Qiutang Zeng, Yang Yu, Liu Yang, Bangwei Wu, Guiwen Yi, Xiaobo Mao and 7 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 153 papers.

0numbers the graph read from it
0cells of the map it votes in
153citing papers in PubMed
12.8field-weighted citation impact, top 1% 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

153 citing papers in PubMed, 231 citations in OpenAlex.

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93 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

17 authors at 3 institutions in 2 countries.

Min ChengDepartment of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China. min_cheng@hust.edu.cn.
Junjie YangDepartment of Biomedical Engineering, University of Alabama at Birmingham, School of Medicine and School of Engineering, 35294, Birmingham, AL, USA.
Xiaoqi ZhaoDepartment of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Eric ZhangDepartment of Biomedical Engineering, University of Alabama at Birmingham, School of Medicine and School of Engineering, 35294, Birmingham, AL, USA.
Qiutang ZengDepartment of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Yang YuDepartment of Biomedical Engineering, University of Alabama at Birmingham, School of Medicine and School of Engineering, 35294, Birmingham, AL, USA.
Liu YangDepartment of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Bangwei WuDepartment of Cardiology, Huashan Hospital, Fudan University, Shanghai, 200040, China.
Guiwen YiDepartment of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Xiaobo MaoDepartment of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Kai HuangDepartment of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Nianguo DongDepartment of Cardiovascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Min XieDivision of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, School of Medicine, Birmingham, 35294, AL, USA.
Nita A LimdiDepartment of Neurology and Epidemiology, University of Alabama at Birmingham, School of Medicine, Birmingham, 35294, AL, USA.
Sumanth D PrabhuDivision of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, School of Medicine, Birmingham, 35294, AL, USA.
Jianyi ZhangDepartment of Biomedical Engineering, University of Alabama at Birmingham, School of Medicine and School of Engineering, 35294, Birmingham, AL, USA.ORCID http://orcid.org/0000-0002-3955-6554
Gangjian QinDepartment of Biomedical Engineering, University of Alabama at Birmingham, School of Medicine and School of Engineering, 35294, Birmingham, AL, USA. gqin@uab.edu.ORCID http://orcid.org/0000-0002-3135-7307
Union Hospital · CNUniversity of Alabama at Birmingham · USFudan University · CN

Funding

Integrated Cellular and Tissue Engineering for Ischemic Heart DiseaseU01HL134764 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BURSAC, NENAD, KAMP, TIMOTHY J. · 2016 to 2022
$7.7M
Endogenous and exogenous mechanisms that promote myocardial remuscularization in post infarction LV remodelingR01HL114120 · NHLBI · UNIVERSITY OF MINNESOTA · PI ZHANG, JIANYI · 2012 to 2021
$5.6M
Role of VCP in coronary ischemic injuryR01HL142291 · NHLBI · LOMA LINDA UNIVERSITY · PI QIU, HONGYU, XIE, ZHONGLIN · 2018 to 2021
$2.6M
E2F2 and Vascular FunctionR01HL138990 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI NAKADA, YUJI · 2017 to 2020
$2.3M
CXCR4 and ckit signaling in BM progenitor cell recruitment in the ischemic heartR01HL113541 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI QIN, GANGJIAN · 2012 to 2015
$1.5M
E2F1 in Cardiac NeovascularizationR01HL093439 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI QIN, GANGJIAN · 2010 to 2013
$1.5M
E2F1 in BM progenitor cell differentiation and cardiovascular repairR01HL131110 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI QIN, GANGJIAN, ZHAO, MING · 2016 to 2019
$1.5M
Patient Oriented Research in Personalized Antithrombotic TherapyK24HL133373 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI LIMDI, NITA A · 2016 to 2025
$1.2M
NHLBI NIH HHS K24 HL133373NHLBI NIH HHS R01 HL093439NHLBI NIH HHS R01 HL113541NHLBI NIH HHS R01 HL114120NHLBI NIH HHS R01 HL131110NHLBI NIH HHS R01 HL138990NHLBI NIH HHS R01 HL142291
6 · The paper itself

Abstract

Myocardial microRNAs (myo-miRs) are released into the circulation after acute myocardial infarction (AMI). How they impact remote organs is however largely unknown. Here we show that circulating myo-miRs are carried in exosomes and mediate functional crosstalk between the ischemic heart and the bone marrow (BM). In mice, we find that AMI is accompanied by an increase in circulating levels of myo-miRs, with miR-1, 208, and 499 predominantly in circulating exosomes and miR-133 in the non-exosomal component. Myo-miRs are imported selectively to peripheral organs and preferentially to the BM. Exosomes mediate the transfer of myo-miRs to BM mononuclear cells (MNCs), where myo-miRs downregulate CXCR4 expression. Injection of exosomes isolated from AMI mice into wild-type mice downregulates CXCR4 expression in BM-MNCs and increases the number of circulating progenitor cells. Thus, we propose that myo-miRs carried in circulating exosomes allow a systemic response to cardiac injury that may be leveraged for cardiac repair.

Indexed as

AgedAnimalsDown-RegulationExosomesFemaleHematopoietic Stem Cell MobilizationHematopoietic Stem CellsHumansMaleMiceMice, Inbred C57BLMicroRNAsMiddle AgedMyocardial InfarctionMyocardiumReceptors, CXCR4CXCR4 protein, mouseMicroRNAsReceptors, CXCR4

Identifiers

PMID30814518
PMCPMC6393447
OpenAlexW2917270161

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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.