Evidence map›Paper›PMID 41128145›Full record

ArticleJournal of the American Heart Association2025

Molecular Mechanisms of Exosomes From Human iPSC-Cardiomyocytes and Mesenchymal Stem Cells in Restoring the Injured Myocardium.

Eileen Tzng, Nathan Bayardo, Gentaro Ikeda, Nirmal Vadgama, Hiroyuki Takashima, Jennifer Lyons, Hirotaka Ieki, Mihoko Bennett, Michael Snyder, Joseph C Wu and 2 more

Abstract read
In one paragraph

Article in Journal of the American Heart Association, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Review
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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.

Eileen TzngDepartment of Medicine Stanford University Stanford California USA.ORCID 0000-0002-7513-9192
Nathan BayardoDepartment of Medicine Stanford University Stanford California USA.ORCID 0000-0001-8574-767X
Gentaro IkedaDepartment of Medicine Stanford University Stanford California USA.ORCID 0000-0003-4019-8990
Nirmal VadgamaCardiovascular Institute Stanford University Stanford California USA.ORCID 0000-0001-6226-3867
Hiroyuki TakashimaDepartment of Medicine Stanford University Stanford California USA.
Jennifer LyonsDepartment of Medicine Stanford University Stanford California USA.
Hirotaka IekiDepartment of Genetics Stanford University Stanford California USA.
Mihoko BennettDepartment of Pediatrics Stanford University Stanford California USA.ORCID 0000-0002-3449-9538
Michael SnyderDepartment of Genetics Stanford University Stanford California USA.ORCID 0000-0003-0784-7987
Joseph C WuCardiovascular Institute Stanford University Stanford California USA.ORCID 0000-0002-6068-8041
Connor G O'BrienDivision of Cardiology, Department of Medicine University of California San Francisco San Francisco California USA.ORCID 0000-0002-2325-8317
Phillip C YangDepartment of Medicine Stanford University Stanford California USA.ORCID 0000-0002-6274-895X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundExosomes are extracellular vesicles 30 to 150 nm in size, mediating the paracrine effects of mesenchymal stem cells (MSCs) and induced pluripotent stem cell-derived cardiomyocytes (iCMs) when used to restore the injured myocardium. While both MSC- and iCM-derived exosomes (MSC-Exo, iCM-Exo) improve cardiac function, their mechanisms of action remain incompletely understood. This study investigates the shared and distinct effects of iCM-Exo and MSC-Exo in a porcine ischemia-reperfusion injury model.

methodsFemale Yorkshire swine underwent proximal left anterior descending artery occlusion with a catheter balloon to induce ischemia-reperfusion injury. Ten 500-μL transendocardial injections delivered a total of 5×10

resultsCardiac MRI revealed that iCM-Exo significantly improved left ventricular ejection fraction, myocardial viability, scar size, and ventricular remodeling compared with MSC-Exo and PBS controls. Transcriptomic analysis revealed both shared and distinct gene expression patterns between the treatments. Shared pathways, including extracellular matrix remodeling and neurovascular integration, contributed to baseline cardiac improvement. Distinct pathways in iCM-Exo treatment involved metabolic reorganization and cardiomyocyte-specific processes, while MSC-Exo emphasized structural stabilization and anti-inflammatory responses.

conclusionsThese findings highlight the complementary roles of iCM-Exo and MSC-Exo in myocardial repair with shared pathways contributing to baseline improvement and distinct pathways driving differences in efficacy. Future studies investigating the potential of combinatorial approaches may provide further insights into optimizing the therapeutic outcomes for patients with heart failure.

Indexed as

ExosomesInduced Pluripotent Stem CellsMesenchymal Stem CellsMesenchymal Stem Cell TransplantationMyocardial InfarctionMyocardial Reperfusion InjuryMyocytes, CardiacAnimalsCells, CulturedDisease Models, AnimalFemaleHumansMyocardiumParacrine CommunicationRecovery of FunctionStroke Volumeexosomesinduced pluripotent stem cellsmesenchymal stem cellsmyocardial infarction

Identifiers

PMID41128145
PMCPMC12684797

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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.