Evidence map›Paper›PMID 35059851›Full record

ArticleCellular and molecular life sciences : CMLS2022

Circulating cardiomyocyte-derived extracellular vesicles reflect cardiac injury during systemic inflammatory response syndrome in mice.

Hargita Hegyesi, Éva Pallinger, Szabina Mecsei, Balázs Hornyák, Csenger Kovácsházi, Gábor B Brenner, Zoltán Giricz, Krisztina Pálóczi, Ágnes Kittel, József Tóvári and 4 more

Open access · hybridAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

28 citing papers in PubMed, 34 citations in OpenAlex.

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  13. Immune mediators in heart-lung communication.Pflugers Archiv : European journal of physiology · 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

14 authors at 4 institutions in 2 countries.

Hargita HegyesiDepartment of Genetics, Cell- and Immunobiology, Semmelweis University, Budapest, Hungary. hegyesi.hargita@med.semmelweis-univ.hu.ORCID http://orcid.org/0000-0002-8800-5169
Éva PallingerDepartment of Genetics, Cell- and Immunobiology, Semmelweis University, Budapest, Hungary.ORCID http://orcid.org/0000-0002-5789-0951
Szabina MecseiDepartment of Genetics, Cell- and Immunobiology, Semmelweis University, Budapest, Hungary.
Balázs HornyákDepartment of Genetics, Cell- and Immunobiology, Semmelweis University, Budapest, Hungary.
Csenger KovácsháziDepartment of Pharmacology and Pharmacotherapy, Semmelweis University, Budapest, Hungary.
Gábor B BrennerDepartment of Pharmacology and Pharmacotherapy, Semmelweis University, Budapest, Hungary.
Zoltán GiriczDepartment of Pharmacology and Pharmacotherapy, Semmelweis University, Budapest, Hungary.
Krisztina PálócziDepartment of Genetics, Cell- and Immunobiology, Semmelweis University, Budapest, Hungary.
Ágnes KittelInstitute of Experimental Medicine, Eötvös Loránd Research Network, Budapest, Hungary.ORCID http://orcid.org/0000-0002-6888-7731
József TóváriDepartment of Experimental Pharmacology, National Institute of Oncology, Budapest, Hungary.ORCID http://orcid.org/0000-0002-5543-3204
Lilla TuriakMS Proteomics Research Group, Research Centre for Natural Sciences, Eötvös Loránd Research Network, Budapest, Hungary.ORCID http://orcid.org/0000-0002-2139-8156
Delaram KhamariDepartment of Genetics, Cell- and Immunobiology, Semmelweis University, Budapest, Hungary.
Péter FerdinandyDepartment of Pharmacology and Pharmacotherapy, Semmelweis University, Budapest, Hungary.ORCID http://orcid.org/0000-0002-6424-6806
Edit I BuzásDepartment of Genetics, Cell- and Immunobiology, Semmelweis University, Budapest, Hungary.ORCID http://orcid.org/0000-0002-3744-206X
Semmelweis University · HUHUN-REN Institute of Experimental Medicine · HUNational Institute of Oncology · HUResearch Network (United States) · US

Funding

horizon 2020 framework programme 739593horizon 2020 framework programme H2020-MSCA-ITN-2017-722148hungarian scientific research fund OTKA K120237nemzeti kutatási, fejlesztési és innovaciós alap Higher Education Excellence Program (FIKP) Therapeutic Thematic Programmenemzeti kutatási, fejlesztési és innovaciós alap NVKP_16-1-2016-0017nemzeti kutatási, fejlesztési és innovaciós alap TKP2020-NKA-26nemzeti kutatási, fejlesztési és innovaciós alap VEKOP-2.3.2-16-2016-000002nemzeti kutatási, fejlesztési és innovaciós alap VEKOP-2.3.3-15-2016-00006nemzeti kutatási, fejlesztési és innovaciós alap VEKOP-2.3.3-15-2017-00016
6 · The paper itself

Abstract

The release of extracellular vesicles (EVs) is increased under cellular stress and cardiomyocyte damaging conditions. However, whether the cardiomyocyte-derived EVs eventually reach the systemic circulation and whether their number in the bloodstream reflects cardiac injury, remains unknown. Wild type C57B/6 and conditional transgenic mice expressing green fluorescent protein (GFP) by cardiomyocytes were studied in lipopolysaccharide (LPS)-induced systemic inflammatory response syndrome (SIRS). EVs were separated both from platelet-free plasma and from the conditioned medium of isolated cardiomyocytes of the left ventricular wall. Size distribution and concentration of the released particles were determined by Nanoparticle Tracking Analysis. The presence of GFP + cardiomyocyte-derived circulating EVs was monitored by flow cytometry and cardiac function was assessed by echocardiography. In LPS-treated mice, systemic inflammation and the consequent cardiomyopathy were verified by elevated plasma levels of TNFα, GDF-15, and cardiac troponin I, and by a decrease in the ejection fraction. Furthermore, we demonstrated elevated levels of circulating small- and medium-sized EVs in the LPS-injected mice. Importantly, we detected GFP

Indexed as

Cell MovementAnimalsClusterinExtracellular VesiclesGlycogen PhosphorylaseGreen Fluorescent ProteinsIntegrasesLipopolysaccharidesMaleMiceMice, Inbred C57BLMice, TransgenicMyocardiumMyocytes, CardiacOrgan SpecificityPhenotypeClu protein, mouseClusterinCre recombinaseGlycogen PhosphorylaseGreen Fluorescent ProteinsIntegrasesLipopolysaccharidesTamoxifenTroponin ICardiomyocyteCardiomyopathyExtracellular vesiclesInducible transgenic miceSIRS

Identifiers

PMID35059851
PMCPMC8776681
OpenAlexW4206079729

What Socratic 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 Socratic graph.