Evidence map›Paper›PMID 33639970›Full record

ArticleJournal of nanobiotechnology2021

Macrophage migration inhibitory factor facilitates the therapeutic efficacy of mesenchymal stem cells derived exosomes in acute myocardial infarction through upregulating miR-133a-3p.

Wenwu Zhu, Ling Sun, Pengcheng Zhao, Yaowu Liu, Jian Zhang, Yuelin Zhang, Yimei Hong, Yeqian Zhu, Yao Lu, Wei Zhao and 2 more

Open access · goldAbstract read
In one paragraph

Article in Journal of nanobiotechnology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed, 3 pooled it
11.4field-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

89 citing papers in PubMed, 3 syntheses or guidelines pooled it, 179 citations in OpenAlex.

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  10. NF-Frontiers in cardiovascular medicine · 2026
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29 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

12 authors at 4 institutions in 1 country.

Wenwu Zhu *Section of Pacing and Electrophysiology, Division of Cardiology, The First Affiliated Hospital With Nanjing Medical University, Nanjing, Guangzhou Road 300, Nanjing, 210029, People's Republic of China.
Ling Sun *Section of Pacing and Electrophysiology, Division of Cardiology, The First Affiliated Hospital With Nanjing Medical University, Nanjing, Guangzhou Road 300, Nanjing, 210029, People's Republic of China.
Pengcheng ZhaoSection of Pacing and Electrophysiology, Division of Cardiology, The First Affiliated Hospital With Nanjing Medical University, Nanjing, Guangzhou Road 300, Nanjing, 210029, People's Republic of China.
Yaowu LiuDepartment of Cardiology, Zhongda Hospital of Southeast University, Nanjing, China.
Jian ZhangSection of Pacing and Electrophysiology, Division of Cardiology, The First Affiliated Hospital With Nanjing Medical University, Nanjing, Guangzhou Road 300, Nanjing, 210029, People's Republic of China.
Yuelin ZhangDepartment of Emergency and Critical Care Medicine, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.
Yimei HongDepartment of Emergency and Critical Care Medicine, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.
Yeqian ZhuSection of Pacing and Electrophysiology, Division of Cardiology, The First Affiliated Hospital With Nanjing Medical University, Nanjing, Guangzhou Road 300, Nanjing, 210029, People's Republic of China.
Yao LuSection of Pacing and Electrophysiology, Division of Cardiology, The First Affiliated Hospital With Nanjing Medical University, Nanjing, Guangzhou Road 300, Nanjing, 210029, People's Republic of China.
Wei ZhaoSection of Pacing and Electrophysiology, Division of Cardiology, The First Affiliated Hospital With Nanjing Medical University, Nanjing, Guangzhou Road 300, Nanjing, 210029, People's Republic of China.
Xinguang ChenSection of Pacing and Electrophysiology, Division of Cardiology, The First Affiliated Hospital With Nanjing Medical University, Nanjing, Guangzhou Road 300, Nanjing, 210029, People's Republic of China.
Fengxiang ZhangSection of Pacing and Electrophysiology, Division of Cardiology, The First Affiliated Hospital With Nanjing Medical University, Nanjing, Guangzhou Road 300, Nanjing, 210029, People's Republic of China. njzfx6@njmu.edu.cn.ORCID http://orcid.org/0000-0003-0125-3926
Nanjing Medical University · CNGuangdong Academy of Medical Sciences · CNChangzhou No.2 People's Hospital · CNZhongda Hospital Southeast University · CN

Funding

National Natural Science Foundation of China 81871113National Natural Science Foundation of China 81901410
6 · The paper itself

Abstract

backgroundExosome transplantation is a promising cell-free therapeutic approach for the treatment of ischemic heart disease. The purpose of this study was to explore whether exosomes derived from Macrophage migration inhibitory factor (MIF) engineered umbilical cord MSCs (ucMSCs) exhibit superior cardioprotective effects in a rat model of AMI and reveal the mechanisms underlying it.

resultsExosomes isolated from ucMSCs (MSC-Exo), MIF engineered ucMSCs (MIF-Exo) and MIF downregulated ucMSCs (siMIF-Exo) were used to investigate cellular protective function in human umbilical vein endothelial cells (HUVECs) and H9C2 cardiomyocytes under hypoxia and serum deprivation (H/SD) and infarcted hearts in rats. Compared with MSC-Exo and siMIF-Exo, MIF-Exo significantly enhanced proliferation, migration, and angiogenesis of HUVECs and inhibited H9C2 cardiomyocyte apoptosis under H/SD in vitro. MIF-Exo also significantly inhibited cardiomyocyte apoptosis, reduced fibrotic area, and improved cardiac function as measured by echocardiography in infarcted rats in vivo. Exosomal miRNAs sequencing and qRT-PCR confirmed miRNA-133a-3p significantly increased in MIF-Exo. The biological effects of HUVECs and H9C2 cardiomyocytes were attenuated with incubation of MIF-Exo and miR-133a-3p inhibitors. These effects were accentuated with incubation of siMIF-Exo and miR-133a-3p mimics that increased the phosphorylation of AKT protein in these cells.

conclusionMIF-Exo can provide cardioprotective effects by promoting angiogenesis, inhibiting apoptosis, reducing fibrosis, and preserving heart function in vitro and in vivo. The mechanism in the biological activities of MIF-Exo involves miR-133a-3p and the downstream AKT signaling pathway.

Indexed as

AnimalsApoptosisCell LineCell ProliferationExosomesHumansHuman Umbilical Vein Endothelial CellsIntramolecular OxidoreductasesMacrophage Migration-Inhibitory FactorsMaleMesenchymal Stem CellsMicroRNAsMyocardial InfarctionMyocardiumMyocytes, CardiacRatsIntramolecular OxidoreductasesMacrophage Migration-Inhibitory FactorsMicroRNAsMif protein, ratMirn133 microRNA, mouseExosomesMacrophage migration inhibitory factorMiR-133a-3pMyocardial infarctionUcMSCs

Identifiers

PMID33639970
PMCPMC7916292
OpenAlexW3128556472

What Socratic holds

Textmetadata
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 Socratic graph.