Evidence map›Paper›PMID 37161563›Full record

ArticleJournal of translational medicine2023

Cardiomyocyte-targeting exosomes from sulforaphane-treated fibroblasts affords cardioprotection in infarcted rats.

Gaia Papini, Giulia Furini, Marco Matteucci, Vanessa Biemmi, Valentina Casieri, Nicole Di Lascio, Giuseppina Milano, Lucia Rosa Chincoli, Francesco Faita, Lucio Barile and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

25 citing papers in PubMed, 25 citations in OpenAlex.

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  17. Exploring the landscape of exosomes in heart failure: a bibliometric analysis.International journal of surgery (London, England) · 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

11 authors at 4 institutions in 2 countries.

Gaia Papini *Unit of Translational Critical Care Medicine, Laboratory of Basic and Applied Medical Sciences, The Interdisciplinary Research Center "Health Science", Scuola Superiore Sant'Anna, Via G. Moruzzi, 1, 56124, Pisa, Italy.
Giulia Furini *Unit of Translational Critical Care Medicine, Laboratory of Basic and Applied Medical Sciences, The Interdisciplinary Research Center "Health Science", Scuola Superiore Sant'Anna, Via G. Moruzzi, 1, 56124, Pisa, Italy.
Marco MatteucciUnit of Translational Critical Care Medicine, Laboratory of Basic and Applied Medical Sciences, The Interdisciplinary Research Center "Health Science", Scuola Superiore Sant'Anna, Via G. Moruzzi, 1, 56124, Pisa, Italy.
Vanessa BiemmiCardiovascular Theranostics, Istituto Cardiocentro Ticino, Laboratories for Translational Research, Ente Ospedaliero Cantonale, Bellinzona, Switzerland.
Valentina CasieriUnit of Translational Critical Care Medicine, Laboratory of Basic and Applied Medical Sciences, The Interdisciplinary Research Center "Health Science", Scuola Superiore Sant'Anna, Via G. Moruzzi, 1, 56124, Pisa, Italy.
Nicole Di LascioUnit of Translational Critical Care Medicine, Laboratory of Basic and Applied Medical Sciences, The Interdisciplinary Research Center "Health Science", Scuola Superiore Sant'Anna, Via G. Moruzzi, 1, 56124, Pisa, Italy.
Giuseppina MilanoCardiovascular Theranostics, Istituto Cardiocentro Ticino, Laboratories for Translational Research, Ente Ospedaliero Cantonale, Bellinzona, Switzerland.
Lucia Rosa ChincoliUnit of Translational Critical Care Medicine, Laboratory of Basic and Applied Medical Sciences, The Interdisciplinary Research Center "Health Science", Scuola Superiore Sant'Anna, Via G. Moruzzi, 1, 56124, Pisa, Italy.
Francesco FaitaInstitute of Clinical Physiology, CNR, Pisa, Italy.
Lucio BarileUnit of Translational Critical Care Medicine, Laboratory of Basic and Applied Medical Sciences, The Interdisciplinary Research Center "Health Science", Scuola Superiore Sant'Anna, Via G. Moruzzi, 1, 56124, Pisa, Italy.
Vincenzo LionettiUnit of Translational Critical Care Medicine, Laboratory of Basic and Applied Medical Sciences, The Interdisciplinary Research Center "Health Science", Scuola Superiore Sant'Anna, Via G. Moruzzi, 1, 56124, Pisa, Italy. v.lionetti@santannapisa.it.ORCID 0000-0002-0640-8651
Scuola Superiore Sant'Anna · ITEnte Ospedaliero Cantonale · CHIstituto di Fisiologia Clinica · ITUniversity of Siena · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundExosomes (EXOs), tiny extracellular vesicles that facilitate cell-cell communication, are being explored as a heart failure treatment, although the features of the cell source restrict their efficacy. Fibroblasts the most prevalent non-myocyte heart cells, release poor cardioprotective EXOs. A noninvasive method for manufacturing fibroblast-derived exosomes (F-EXOs) that target cardiomyocytes and slow cardiac remodeling is expected. As a cardioprotective isothiocyanate, sulforaphane (SFN)-induced F-EXOs (SFN-F-EXOs) should recapitulate its anti-remodeling properties.

methodsExosomes from low-dose SFN (3 μM/7 days)-treated NIH/3T3 murine cells were examined for number, size, and protein composition. Fluorescence microscopy, RT-qPCR, and western blot assessed cell size, oxidative stress, AcH4 levels, hypertrophic gene expression, and caspase-3 activation in angiotensin II (AngII)-stressed HL-1 murine cardiomyocytes 12 h-treated with various EXOs. The uptake of fluorescently-labeled EXOs was also measured in cardiomyocytes. The cardiac function of infarcted male Wistar rats intramyocardially injected with different EXOs (1·10

resultsSustained treatment of NIH/3T3 with non-toxic SFN concentration significantly enhances the release of CD81 + EXOs rich in TSG101 (Tumor susceptibility gene 101) and Hsp70 (Heat Shock Protein 70), and containing maspin, an endogenous histone deacetylase 1 inhibitor. SFN-F-EXOs counteract angiotensin II (AngII)-induced hypertrophy and apoptosis in murine HL-1 cardiomyocytes enhancing SERCA2a (sarcoplasmic/endoplasmic reticulum Ca

conclusionsLong-term low-dose SFN treatment of fibroblasts enhances the release of anti-remodeling cardiomyocyte-targeted F-EXOs, which effectively prevent the onset of HF. The proposed method opens a new avenue for large-scale production of cardioprotective exosomes for clinical application using allogeneic fibroblasts.

Indexed as

ExosomesMyocytes, CardiacAngiotensin IIAnimalsAntibodiesFibroblastsIsothiocyanatesMaleMiceRatsRats, WistarSulfoxidesAngiotensin IIAntibodiesIsothiocyanatessulforaphaneSulfoxidesAllogeneic fibroblastCardioprotectionExosomesMyocardial infarctionRemodelingSulforaphane (PubChem CID: 5350)

Identifiers

PMID37161563
PMCPMC10169450
OpenAlexW4376115682

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.