Evidence map›Paper›PMID 35319169›Full record

ArticleJournal of cachexia, sarcopenia and muscle2022

A negative feedback loop between fibroadipogenic progenitors and muscle fibres involving endothelin promotes human muscle fibrosis.

Mona Bensalah, Laura Muraine, Alexis Boulinguiez, Lorenzo Giordani, Victorine Albert, Victor Ythier, Jamila Dhiab, Alison Oliver, Valentine Hanique, Teresa Gidaro and 8 more

Open access · goldAbstract read
In one paragraph

Article in Journal of cachexia, sarcopenia and muscle, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

21 citing papers in PubMed, 28 citations in OpenAlex.

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  10. Thrown for a loop: fibro-adipogenic progenitors in skeletal muscle fibrosis.American journal of physiology. Cell physiology · 2023
    Review
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  14. Altered muscle niche contributes to myogenic deficit in the D2-bioRxiv : the preprint server for biology · 2023
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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

18 authors at 2 institutions in 1 country.

Mona BensalahSorbonne Université, Inserm, Institut de Myologie, Centre de Recherche en Myologie, Paris, France.ORCID 0000-0003-2589-8657
Laura MuraineSorbonne Université, Inserm, Institut de Myologie, Centre de Recherche en Myologie, Paris, France.
Alexis BoulinguiezSorbonne Université, Inserm, Institut de Myologie, Centre de Recherche en Myologie, Paris, France.ORCID 0000-0001-6886-6140
Lorenzo GiordaniSorbonne Université, Inserm, Institut de Myologie, Centre de Recherche en Myologie, Paris, France.ORCID 0000-0002-3417-2965
Victorine AlbertSorbonne Université, Inserm, Institut de Myologie, Centre de Recherche en Myologie, Paris, France.
Victor YthierSorbonne Université, Inserm, Institut de Myologie, Centre de Recherche en Myologie, Paris, France.
Jamila DhiabSorbonne Université, Inserm, Institut de Myologie, Centre de Recherche en Myologie, Paris, France.
Alison OliverSorbonne Université, Inserm, Institut de Myologie, Centre de Recherche en Myologie, Paris, France.
Valentine HaniqueSorbonne Université, Inserm, Institut de Myologie, Centre de Recherche en Myologie, Paris, France.
Teresa GidaroSorbonne Université, Inserm, Institut de Myologie, Centre de Recherche en Myologie, Paris, France.
Sophie PeriéSorbonne Université, Inserm, Institut de Myologie, Centre de Recherche en Myologie, Paris, France.ORCID 0000-0002-3412-0700
Jean Lacau St-GuilySorbonne Université, Inserm, Institut de Myologie, Centre de Recherche en Myologie, Paris, France.ORCID 0000-0003-4005-5957
Aurélien CorneauUMS037, PASS, Plateforme de Cytométrie de la Pitié-Salpêtrière CyPS, Sorbonne Université, Paris, France.ORCID 0000-0003-1272-6872
Gillian Butler-BrowneSorbonne Université, Inserm, Institut de Myologie, Centre de Recherche en Myologie, Paris, France.
Anne BigotSorbonne Université, Inserm, Institut de Myologie, Centre de Recherche en Myologie, Paris, France.ORCID 0000-0003-0337-5425
Vincent MoulySorbonne Université, Inserm, Institut de Myologie, Centre de Recherche en Myologie, Paris, France.ORCID 0000-0003-3809-4033
Elisa NegroniSorbonne Université, Inserm, Institut de Myologie, Centre de Recherche en Myologie, Paris, France.ORCID 0000-0001-8302-2544
Capucine TrolletSorbonne Université, Inserm, Institut de Myologie, Centre de Recherche en Myologie, Paris, France.ORCID 0000-0002-4838-3712
Inserm · FRSorbonne Université · FR

Funding

Association Française contre les Myopathies (AFM-Téléthon) eOPMD 17110Fondation Recherche Médicale EQU201903007784Institut national de la santé et de la recherche médicale (INSERM), Sorbonne University SU-16-R-EMR-60 Fibe-CellSorbonne University SU-16-R-EMR-60 Fib-Cell
6 · The paper itself

Abstract

backgroundFibrosis is defined as an excessive accumulation of extracellular matrix (ECM) components. Many organs are subjected to fibrosis including the lung, liver, heart, skin, kidney, and muscle. Muscle fibrosis occurs in response to trauma, aging, or dystrophies and impairs muscle function. Fibrosis represents a hurdle for the treatment of human muscular dystrophies. While data on the mechanisms of fibrosis have mostly been investigated in mice, dystrophic mouse models often do not recapitulate fibrosis as observed in human patients. Consequently, the cellular and molecular mechanisms that lead to fibrosis in human muscle still need to be identified.

methodsCombining mass cytometry, transcriptome profiling, in vitro co-culture experiments, and in vivo transplantation in immunodeficient mice, we investigated the role and nature of nonmyogenic cells (fibroadipogenic progenitors, FAPs) from human fibrotic muscles of healthy individuals (FibM

resultsWe found that the proliferation rate of FAPs from fibrotic muscle is 3-4 times higher than those of FAPs from nonfibrotic muscle (population doubling per day: M

conclusionsOur data demonstrate the key role of FAPs and their cross-talk with muscle cells through a paracrine signalling pathway in fibrosis of human skeletal muscle and identify endothelin as a new druggable target to counteract human muscle fibrosis.

Indexed as

AdipogenesisMuscular Dystrophy, OculopharyngealAnimalsEndothelinsFeedbackFibrosisHumansMiceMuscle Fibers, SkeletalMuscle, SkeletalTransforming Growth Factor betaEndothelinsTransforming Growth Factor betaECMEndothelinFAPsFibrosisHumanPharyngeal muscleRegenerationSkeletal muscleTGFβ

Identifiers

PMID35319169
PMCPMC9178170
OpenAlexW4221044901

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.