Evidence map›Paper›PMID 33797200›Full record

ArticleJournal of cellular and molecular medicine2021

Exosomes from neuronal stem cells may protect the heart from ischaemia/reperfusion injury via JAK1/2 and gp130.

Miroslava Katsur, Zhenhe He, Vladimir Vinokur, Randolph Corteling, Derek M Yellon, Sean M Davidson

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 17% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

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  13. Clinical applications of stem cell-derived exosomes.Signal transduction and targeted therapy · 2024
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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

6 authors at 3 institutions in 2 countries.

Miroslava KatsurThe Hatter Cardiovascular Institute, University College London, London, UK.
Zhenhe HeThe Hatter Cardiovascular Institute, University College London, London, UK.
Vladimir VinokurDepartment of Biochemistry and Molecular Biology, Institute of Medical Research Israel-Canada, The Hebrew University of Jerusalem, Jerusalem, Israel.
Randolph CortelingReNeuron Ltd, Pencoed, Bridgend, UK.
Derek M YellonThe Hatter Cardiovascular Institute, University College London, London, UK.ORCID 0000-0001-7791-9320
Sean M DavidsonThe Hatter Cardiovascular Institute, University College London, London, UK.ORCID 0000-0001-5182-4980
University College London · GBHebrew University of Jerusalem · ILReNeuron (United Kingdom) · GB

Funding

Biomedical Research Council BRC233/CM/SD/101320British Heart Foundation PG/19/51/34493Medical Research Council MR/N013867/1NIHR
6 · The paper itself

Abstract

Myocardial infarction requires urgent reperfusion to salvage viable heart tissue. However, reperfusion increases infarct size further by promoting mitochondrial damage in cardiomyocytes. Exosomes from a wide range of different cell sources have been shown to activate cardioprotective pathways in cardiomyocytes, thereby reducing infarct size. Yet, it is currently challenging to obtain highly pure exosomes in quantities enough for clinical studies. To overcome this problem, we used exosomes isolated from CTX0E03 neuronal stem cells, which are genetically stable, conditionally inducible and can be produced on an industrial scale. However, it is unknown whether exosomes from neuronal stem cells may reduce cardiac ischaemia/reperfusion injury. In this study, we demonstrate that exosomes from differentiating CTX0E03 cells can reduce infarct size in mice. In an in vitro assay, these exosomes delayed cardiomyocyte mitochondrial permeability transition pore opening, which is responsible for cardiomyocyte death after reperfusion. The mechanism of MPTP inhibition was via gp130 signalling and the downstream JAK/STAT pathway. Our results support previous findings that exosomes from non-cardiomyocyte-related cells produce exosomes capable of protecting cardiomyocytes from myocardial infarction. We anticipate our findings may encourage scientists to use exosomes obtained from reproducible clinical-grade stocks of cells for their ischaemia/reperfusion studies.

Indexed as

AnimalsCytokine Receptor gp130ExosomesGene Expression RegulationJanus Kinase 1Janus Kinase 2MaleMiceMice, Inbred C57BLMyocardial InfarctionMyocardial Reperfusion InjuryNeural Stem CellsProtective AgentsCytokine Receptor gp130Il6st protein, mouseJak1 protein, mouseJak2 protein, mouseJanus Kinase 1Janus Kinase 2Protective Agentscardiacexosomesextracellular vesiclesinfarctionischaemia and reperfusionmitochondrianeuronal stem cells

Identifiers

PMID33797200
PMCPMC8093960
OpenAlexW3150955351

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.