Evidence map›Paper›PMID 30634641›Full record

ArticleAntioxidants (Basel, Switzerland)2019

Modification of Cardiac Progenitor Cell-Derived Exosomes by miR-322 Provides Protection against Myocardial Infarction through Nox2-Dependent Angiogenesis.

Seock-Won Youn, Yang Li, Young-Mee Kim, Varadarajan Sudhahar, Kareem Abdelsaid, Ha Won Kim, Yutao Liu, David J R Fulton, Muhammad Ashraf, Yaoliang Tang and 2 more

Open access · goldAbstract read
In one paragraph

Article in Antioxidants (Basel, Switzerland), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 1 pooled it
3.9field-weighted citation impact, top 5% 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

54 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.

  1. Pooled it
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  8. Therapeutic application of extracellular vesicles in human diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Review
  9. Extracellular vesicle therapeutics for cardiac repair.Journal of molecular and cellular cardiology · 2025
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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

12 authors at 1 institution in 1 country.

Seock-Won YounVascular Biology Center, Medical College of Georgia at Augusta University, Augusta, GA 30912, USA. swyoun93@gmail.com.
Yang LiVascular Biology Center, Medical College of Georgia at Augusta University, Augusta, GA 30912, USA. yanli@augusta.edu.
Young-Mee KimVascular Biology Center, Medical College of Georgia at Augusta University, Augusta, GA 30912, USA. ymkim@augusta.edu.
Varadarajan SudhaharVascular Biology Center, Medical College of Georgia at Augusta University, Augusta, GA 30912, USA. svaradarajan@augusta.edu.
Kareem AbdelsaidVascular Biology Center, Medical College of Georgia at Augusta University, Augusta, GA 30912, USA. kabdelsaid@augusta.edu.ORCID 0000-0002-1528-1517
Ha Won KimVascular Biology Center, Medical College of Georgia at Augusta University, Augusta, GA 30912, USA. hkim3@augusuta.edu.ORCID 0000-0001-6272-4248
Yutao LiuDepartment of Cellular Biology & Anatomy, Augusta University, Augusta, GA 30912, USA. yutliu@augusta.edu.
David J R FultonVascular Biology Center, Medical College of Georgia at Augusta University, Augusta, GA 30912, USA. dfulton@augusta.edu.ORCID 0000-0002-1528-1517
Muhammad AshrafVascular Biology Center, Medical College of Georgia at Augusta University, Augusta, GA 30912, USA. mashraf@augusta.edu.
Yaoliang TangVascular Biology Center, Medical College of Georgia at Augusta University, Augusta, GA 30912, USA. yaotang@augusta.edu.
Tohru FukaiVascular Biology Center, Medical College of Georgia at Augusta University, Augusta, GA 30912, USA. tfukai@augusta.edu.
Masuko Ushio-FukaiVascular Biology Center, Medical College of Georgia at Augusta University, Augusta, GA 30912, USA. mfukai@augusta.edu.
Augusta University · US

Funding

Vascular Extracellular Superoxide Dismutase ModulationR01HL070187 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI FUKAI, TOHRU · 2002 to 2017
$4.2M
Copper transport protein and inflammatory angiogenesisR01HL116976 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI FUKAI, TOHRU, USHIO-FUKAI, MASUKO · 2013 to 2016
$2.9M
Cu Transporting ATPase and Diabetic Vascular ComplicationsR01HL133613 · NHLBI · AUGUSTA UNIVERSITY · PI FUKAI, TOHRU, USHIO-FUKAI, MASUKO · 2017 to 2020
$2.7M
Protein Disulfide Isomerase as Novel Redox Sensor in VEGF SignalingR01HL135584 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI USHIO-FUKAI, MASUKO · 2017 to 2020
$1.5M
NIH HHS NIHR01HL070187NIH HHS NIHR01HL116976NIH HHS NIHR01HL133613NIH HHS NIHR01HL134354NIH HHS NIHR01HL135584U.S. Department of Veterans Affairs 2I01BX001232
6 · The paper itself

Abstract

Myocardial infarction (MI) is the primary cause of cardiovascular mortality, and therapeutic strategies to prevent or mitigate the consequences of MI are a high priority. Cardiac progenitor cells (CPCs) have been used to treat cardiac injury post-MI, and despite poor engraftment, they have been shown to inhibit apoptosis and to promote angiogenesis through poorly understood paracrine effects. We previously reported that the direct injection of exosomes derived from CPCs (CPCexo) into mouse hearts provides protection against apoptosis in a model of acute ischemia/reperfusion injury. Moreover, we and others have reported that reactive oxygen species (ROS) derived from NADPH oxidase (NOX) can enhance angiogenesis in endothelial cells (ECs). Here we examined whether bioengineered CPCexo transfected with a pro-angiogenic miR-322 (CPCexo-322) can improve therapeutic efficacy in a mouse model of MI as compared to CPCexo. Systemic administration of CPCexo-322 in mice after ischemic injury provided greater protection post-MI than control CPCexo, in part, through enhanced angiogenesis in the border zones of infarcted hearts. Mechanistically, the treatment of cultured human ECs with CPCexo-322 resulted in a greater angiogenic response, as determined by increased EC migration and capillary tube formation via increased Nox2-derived ROS. Our study reveals that the engineering of CPCexo via microRNA (miR) programing can enhance angiogenesis, and this may be an effective therapeutic strategy for the treatment of ischemic cardiovascular diseases.

Indexed as

angiogenesiscardiac progenitor cellexosomemiR-322myocardial infarctionNADPH oxidasereactive oxygen species

Identifiers

PMID30634641
PMCPMC6356993
OpenAlexW2908756338

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.