Evidence map›Paper›PMID 33668142›Full record

ArticleInternational journal of molecular sciences2021

Selective Cardiomyocyte Oxidative Stress Leads to Bystander Senescence of Cardiac Stromal Cells.

Hélène Martini, Lise Lefevre, Sylvain Sayir, Romain Itier, Damien Maggiorani, Marianne Dutaur, Dimitri J Marsal, Jérôme Roncalli, Nathalie Pizzinat, Daniel Cussac and 3 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

9 citing papers in PubMed, 15 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

13 authors at 2 institutions in 1 country.

Hélène MartiniInstitute of Metabolic and Cardiovascular Diseases (I2MC), Inserm UMR 1048, University of Toulouse, 31400 Toulouse, France.
Lise LefevreInstitute of Metabolic and Cardiovascular Diseases (I2MC), Inserm UMR 1048, University of Toulouse, 31400 Toulouse, France.
Sylvain SayirInstitute Cardiomet, FHU IMPACT, University Hospital of Toulouse, 31400 Toulouse, France.
Romain ItierInstitute Cardiomet, FHU IMPACT, University Hospital of Toulouse, 31400 Toulouse, France.ORCID 0000-0002-3972-0545
Damien MaggioraniInstitute of Metabolic and Cardiovascular Diseases (I2MC), Inserm UMR 1048, University of Toulouse, 31400 Toulouse, France.
Marianne DutaurInstitute of Metabolic and Cardiovascular Diseases (I2MC), Inserm UMR 1048, University of Toulouse, 31400 Toulouse, France.
Dimitri J MarsalInstitute of Metabolic and Cardiovascular Diseases (I2MC), Inserm UMR 1048, University of Toulouse, 31400 Toulouse, France.ORCID 0000-0001-5518-5514
Jérôme RoncalliInstitute of Metabolic and Cardiovascular Diseases (I2MC), Inserm UMR 1048, University of Toulouse, 31400 Toulouse, France.ORCID 0000-0002-4093-0435
Nathalie PizzinatInstitute of Metabolic and Cardiovascular Diseases (I2MC), Inserm UMR 1048, University of Toulouse, 31400 Toulouse, France.ORCID 0000-0002-4823-1743
Daniel CussacInstitute of Metabolic and Cardiovascular Diseases (I2MC), Inserm UMR 1048, University of Toulouse, 31400 Toulouse, France.ORCID 0000-0002-7227-898X
Angelo PariniInstitute of Metabolic and Cardiovascular Diseases (I2MC), Inserm UMR 1048, University of Toulouse, 31400 Toulouse, France.
Jeanne Mialet-PerezInstitute of Metabolic and Cardiovascular Diseases (I2MC), Inserm UMR 1048, University of Toulouse, 31400 Toulouse, France.
Victorine Douin-EchinardInstitute of Metabolic and Cardiovascular Diseases (I2MC), Inserm UMR 1048, University of Toulouse, 31400 Toulouse, France.ORCID 0000-0002-0630-7666
Inserm · FRInstitut de Mathématiques de Toulouse · FR

Funding

Conseil Régional Midi-Pyrénées APRTCN MiPyEuropean Regional Development Fund program INSPIRE (FEDER-région Occitanie)Fédération Française de Cardiologie fellowships and fundingInstitut National de la Santé et de la Recherche Médicale ANR
6 · The paper itself

Abstract

Accumulation of senescent cells in tissues during normal or accelerated aging has been shown to be detrimental and to favor the outcomes of age-related diseases such as heart failure (HF). We have previously shown that oxidative stress dependent on monoamine oxidase A (MAOA) activity in cardiomyocytes promotes mitochondrial damage, the formation of telomere-associated foci, senescence markers, and triggers systolic cardiac dysfunction in a model of transgenic mice overexpressing MAOA in cardiomyocytes (Tg MAOA). However, the impact of cardiomyocyte oxidative stress on the cardiac microenvironment in vivo is still unclear. Our results showed that systolic cardiac dysfunction in Tg MAOA mice was strongly correlated with oxidative stress induced premature senescence of cardiac stromal cells favoring the recruitment of CCR2

Indexed as

Bystander EffectCellular SenescenceOxidative StressAgingAnimalsCells, CulturedDNA DamageMaleMiceMice, Inbred C57BLMice, TransgenicMonoamine OxidaseMyocytes, CardiacStromal CellsMonoamine Oxidasecardiac mesenchymal stromal cellsCCR2+ Macrophagesmonoamine oxidase Aoxidative stressSASPstress-induced premature senescence

Identifiers

PMID33668142
PMCPMC7956294
OpenAlexW3132670140

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.