Evidence map›Paper›PMID 30755583›Full record

ArticleExperimental & molecular medicine2019

In vivo transduction of ETV2 improves cardiac function and induces vascular regeneration following myocardial infarction.

Sunghun Lee, Dong Hun Lee, Bong-Woo Park, Riyoun Kim, Anh Duc Hoang, Sang-Keun Woo, Wenjun Xiong, Yong Jin Lee, Kiwon Ban, Hun-Jun Park

Erratum issuedAbstract read
In one paragraph

Article in Experimental & molecular medicine, 2019. 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 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed.

  1. Article
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  3. mRNA-basedMolecular therapy. Nucleic acids · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors.

Sunghun Lee *Department of Biomedical Sciences, City University of Hong Kong, Kowloon Tong, Hong Kong.ORCID http://orcid.org/0000-0003-3374-2070
Dong Hun Lee *Department of Pediatrics, Children's Heart Research and Outcomes Center, Emory University School of Medicine, Atlanta, GA, USA.
Bong-Woo Park *Department of Medical Life Science, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.
Riyoun KimDepartment of Biomedical Sciences, City University of Hong Kong, Kowloon Tong, Hong Kong.
Anh Duc HoangDepartment of Biomedical Sciences, City University of Hong Kong, Kowloon Tong, Hong Kong.
Sang-Keun WooDivision of RI-Convergence Research, Korea Institute of Radiological and Medical Sciences, Seoul, Republic of Korea.
Wenjun XiongDepartment of Biomedical Sciences, City University of Hong Kong, Kowloon Tong, Hong Kong.
Yong Jin LeeDivision of RI-Convergence Research, Korea Institute of Radiological and Medical Sciences, Seoul, Republic of Korea.
Kiwon BanDepartment of Biomedical Sciences, City University of Hong Kong, Kowloon Tong, Hong Kong. ban.kw@cityu.edu.hk.ORCID http://orcid.org/0000-0003-0805-5439
Hun-Jun ParkDepartment of Medical Life Science, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea. cardioman@catholic.ac.kr.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vascular regeneration in ischemic hearts has been considered a target for new therapeutic strategies. It has been reported that ETV2 is essential for vascular development, injury-induced neovascularization and direct cell reprogramming of non-endothelial cells into endothelial cells. Thus, the objective of this study was to explore the therapeutic potential of ETV2 in murine models of myocardial infarction in vivo. Direct myocardial delivery of lentiviral ETV2 into rodents undergoing myocardial infarction dramatically upregulated the expression of markers for angiogenesis as well as anti-fibrosis and anti-inflammatory factors in vivo. Consistent with these findings, echocardiography showed significantly improved cardiac function in hearts with induced myocardial infarction upon ETV2 injection compared to that in the control virus-injected group as determined by enhanced ejection fraction and fractional shortening. In addition, ETV2-injected hearts were protected against massive fibrosis with a remarkable increase in capillary density. Interestingly, major fractions of capillaries were stained positive for ETV2. In addition, ECs infected with ETV2 showed enhanced proliferation, suggesting a direct role of ETV2 in vascular regeneration in diseased hearts. Furthermore, culture media from ETV2-overexpressing cardiac fibroblasts promoted endothelial cell migration based on scratch assay. Importantly, intramyocardial injection of the adeno-associated virus form of ETV2 into rat hearts with induced myocardial infarction designed for clinical applicability consistently resulted in significant augmentation of cardiac function. We provide compelling evidence that ETV2 has a robust effect on vascular regeneration and enhanced cardiac repair after myocardial infarction, highlighting a potential therapeutic function of ETV2 as an efficient means to treat failing hearts.

Indexed as

Transduction, GeneticAnimalsCell LineCell MovementCell ProliferationDependovirusDisease Models, AnimalEchocardiographyEndothelial CellsFibroblastsFibrosisFluorodeoxyglucose F18Gene ExpressionGenetic VectorsHumansImmunohistochemistryETV2 protein, humanFluorodeoxyglucose F18Transcription Factors

Identifiers

PMID30755583
PMCPMC6372609

What OpenQuestion holds

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Registered trials

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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.