Evidence map›Paper›PMID 33396724›Full record

ArticleInternational journal of molecular sciences2020

Lamin-Related Congenital Muscular Dystrophy Alters Mechanical Signaling and Skeletal Muscle Growth.

Daniel J Owens, Julien Messéant, Sophie Moog, Mark Viggars, Arnaud Ferry, Kamel Mamchaoui, Emmanuelle Lacène, Norma Roméro, Astrid Brull, Gisèle Bonne and 2 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

23 citing papers in PubMed, 31 citations in OpenAlex.

  1. Junctions in Jeopardy: the neuromuscular junction is a selective pathological target in Charcot-Marie-Tooth disease.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
    Review
  2. Article
  3. Precise gene editing of pathogenic Lamin A mutations corrects cardiac disease.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
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  7. Review
  8. Review
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  15. Article
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  18. The Neuromuscular Junction: Roles in Aging and Neuromuscular Disease.International journal of molecular sciences · 2021
    Review
  19. Review
  20. Review
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 3 institutions in 2 countries.

Daniel J OwensCenter for Research in Myology, Sorbonne Université, INSERM UMRS_974, 75013 Paris, France.ORCID 0000-0002-1908-8677
Julien MesséantCenter for Research in Myology, Sorbonne Université, INSERM UMRS_974, 75013 Paris, France.
Sophie MoogInovarion, 75005 Paris, France.
Mark ViggarsResearch Institute for Sport and Exercise Science, Liverpool John Moores University, Liverpool L3 3AF, UK.
Arnaud FerryCenter for Research in Myology, Sorbonne Université, INSERM UMRS_974, 75013 Paris, France.
Kamel MamchaouiCenter for Research in Myology, Sorbonne Université, INSERM UMRS_974, 75013 Paris, France.
Emmanuelle LacèneNeuromuscular Morphology Unit, Institute of Myology, Pitié-Salpêtrière Hospital, 75013 Paris, France.ORCID 0000-0002-0675-7309
Norma RoméroNeuromuscular Morphology Unit, Institute of Myology, Pitié-Salpêtrière Hospital, 75013 Paris, France.
Astrid BrullCenter for Research in Myology, Sorbonne Université, INSERM UMRS_974, 75013 Paris, France.ORCID 0000-0002-3012-451X
Gisèle BonneCenter for Research in Myology, Sorbonne Université, INSERM UMRS_974, 75013 Paris, France.ORCID 0000-0002-2516-3258
Gillian Butler-BrowneCenter for Research in Myology, Sorbonne Université, INSERM UMRS_974, 75013 Paris, France.
Catherine CoiraultCenter for Research in Myology, Sorbonne Université, INSERM UMRS_974, 75013 Paris, France.ORCID 0000-0002-5594-1057
Inserm · FRSorbonne Université · FRLiverpool John Moores University · GB

Funding

ANR Sorbonne-University ANR-11-IDEX-0004-02
6 · The paper itself

Abstract

Laminopathies are a clinically heterogeneous group of disorders caused by mutations in the

Indexed as

MutationSignal TransductionAnimalsBiopsyCell CommunicationCell Cycle ProteinsDisease Models, AnimalFluorescent Antibody TechniqueGene ExpressionGenetic Association StudiesGenetic Predisposition to DiseaseGenotypeHumansLamin Type AMiceMuscle Fibers, SkeletalCell Cycle ProteinsLamin Type ATranscription FactorsYY1AP1 protein, humanmechanotransductionmuscle growthnuclear envelopesatellite cellYAP

Identifiers

PMID33396724
PMCPMC7795708
OpenAlexW3116963028

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.