Evidence map›Paper›PMID 36831249›Full record

ArticleCells2023

Transfer of Cardiac Mitochondria Improves the Therapeutic Efficacy of Mesenchymal Stem Cells in a Preclinical Model of Ischemic Heart Disease.

Marie-Luce Vignais, Jennyfer Levoux, Pierre Sicard, Khattar Khattar, Catherine Lozza, Marianne Gervais, Safia Mezhoud, Jean Nakhle, Frederic Relaix, Onnik Agbulut and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

18 citing papers in PubMed, 18 citations in OpenAlex.

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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 2 institutions in 1 country.

Marie-Luce VignaisInstitut de Génomique Fonctionnelle, University Montpellier, CNRS, INSERM, 34094 Montpellier, France.ORCID 0000-0002-0183-5953
Jennyfer LevouxUniversité Paris-Est Créteil, INSERM, IMRB, 94010 Créteil, France.
Pierre SicardPhyMedExp, Inserm, CNRS, University of Montpellier, 34295 Montpellier, France.ORCID 0000-0001-5837-3916
Khattar KhattarInstitut de Génomique Fonctionnelle, University Montpellier, CNRS, INSERM, 34094 Montpellier, France.
Catherine LozzaPhyMedExp, Inserm, CNRS, University of Montpellier, 34295 Montpellier, France.ORCID 0000-0002-6751-7042
Marianne GervaisUniversité Paris-Est Créteil, INSERM, IMRB, 94010 Créteil, France.
Safia MezhoudUniversité Paris-Est Créteil, INSERM, IMRB, 94010 Créteil, France.
Jean NakhleInstitut de Génomique Fonctionnelle, University Montpellier, CNRS, INSERM, 34094 Montpellier, France.
Frederic RelaixUniversité Paris-Est Créteil, INSERM, IMRB, 94010 Créteil, France.ORCID 0000-0003-1270-1472
Onnik AgbulutSorbonne Université, Institut de Biologie Paris-Seine (IBPS), CNRS UMR 8256, INSERM U1164, Biological Adaptation and Ageing, 75005 Paris, France.
Jeremy FauconnierPhyMedExp, Inserm, CNRS, University of Montpellier, 34295 Montpellier, France.ORCID 0000-0003-2748-0983
Anne-Marie RodriguezUniversité Paris-Est Créteil, INSERM, IMRB, 94010 Créteil, France.ORCID 0000-0001-5557-8975
Centre National de la Recherche Scientifique · FRInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe use of mesenchymal stem cells (MSCs) appears to be a promising therapeutic approach for cardiac repair after myocardial infarction. However, clinical trials have revealed the need to improve their therapeutic efficacy. Recent evidence demonstrated that mitochondria undergo spontaneous transfer from damaged cells to MSCs, resulting in the activation of the cytoprotective and pro-angiogenic functions of recipient MSCs. Based on these observations, we investigated whether the preconditioning of MSCs with mitochondria could optimize their therapeutic potential for ischemic heart disease.

methodsHuman MSCs were exposed to mitochondria isolated from human fetal cardiomyocytes. After 24 h, the effects of mitochondria preconditioning on the MSCs' function were analyzed both in vitro and in vivo.

resultsWe found that cardiac mitochondria-preconditioning improved the proliferation and repair properties of MSCs in vitro. Mechanistically, cardiac mitochondria mediate their stimulatory effects through the production of reactive oxygen species, which trigger their own degradation in recipient MSCs. These effects were further confirmed in vivo, as the mitochondria preconditioning of MSCs potentiated their therapeutic efficacy on cardiac function following their engraftment into infarcted mouse hearts.

conclusionsThe preconditioning of MSCs with the artificial transfer of cardiac mitochondria appears to be promising strategy to improve the efficacy of MSC-based cell therapy in ischemic heart disease.

Indexed as

Mesenchymal Stem CellsMyocardial InfarctionMyocardial IschemiaAnimalsHumansMiceMitochondria, HeartMyocytes, Cardiaccell therapymesenchymal stem cellsmetabolismmitochondria transferpost-ischemic heart failure

Identifiers

PMID36831249
PMCPMC9953768
OpenAlexW4320492258

What OpenQuestion 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 OpenQuestion graph.