Evidence map›Paper›PMID 33078583›Full record

ArticleJournal of cachexia, sarcopenia and muscle2020

Cell autonomous requirement of neurofibromin (Nf1) for postnatal muscle hypertrophic growth and metabolic homeostasis.

Xiaoyan Wei, Julia Franke, Mario Ost, Kristina Wardelmann, Stefan Börno, Bernd Timmermann, David Meierhofer, Andre Kleinridders, Susanne Klaus, Sigmar Stricker

Open access · goldAbstract read
In one paragraph

Article in Journal of cachexia, sarcopenia and muscle, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

7 citing papers in PubMed, 13 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

10 authors at 3 institutions in 1 country.

Xiaoyan WeiMusculoskeletal Development and Regeneration Group, Institute of Chemistry and Biochemistry, Freie Universität Berlin, Berlin, Germany.
Julia FrankeMusculoskeletal Development and Regeneration Group, Institute of Chemistry and Biochemistry, Freie Universität Berlin, Berlin, Germany.
Mario OstDepartment of Physiology of Energy Metabolism, German Institute for Human Nutrition, Nuthetal, Germany.ORCID 0000-0002-1811-2049
Kristina WardelmannJunior Research Group Central Regulation of Metabolism, German Institute for Human Nutrition, Nuthetal, Germany.
Stefan BörnoSequencing Core Unit, Max Planck Institute for Molecular Genetics, Berlin, Germany.
Bernd TimmermannSequencing Core Unit, Max Planck Institute for Molecular Genetics, Berlin, Germany.
David MeierhoferMass Spectrometry Core Unit, Max Planck Institute for Molecular Genetics, Berlin, Germany.ORCID 0000-0002-0170-868X
Andre KleinriddersJunior Research Group Central Regulation of Metabolism, German Institute for Human Nutrition, Nuthetal, Germany.ORCID 0000-0002-4248-6366
Susanne KlausDepartment of Physiology of Energy Metabolism, German Institute for Human Nutrition, Nuthetal, Germany.ORCID 0000-0001-8726-185X
Sigmar StrickerMusculoskeletal Development and Regeneration Group, Institute of Chemistry and Biochemistry, Freie Universität Berlin, Berlin, Germany.ORCID 0000-0002-7174-5363
Max Planck Institute for Molecular Genetics · DEUniversity of Potsdam · DEUniversity Hospital Leipzig · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNeurofibromatosis type 1 (NF1) is a multi-organ disease caused by mutations in neurofibromin 1 (NF1). Amongst other features, NF1 patients frequently show reduced muscle mass and strength, impairing patients' mobility and increasing the risk of fall. The role of Nf1 in muscle and the cause for the NF1-associated myopathy are mostly unknown.

methodsTo dissect the function of Nf1 in muscle, we created muscle-specific knockout mouse models for NF1, inactivating Nf1 in the prenatal myogenic lineage either under the Lbx1 promoter or under the Myf5 promoter. Mice were analysed during prenatal and postnatal myogenesis and muscle growth.

resultsNf1

conclusionsOur results demonstrate a cell autonomous role for Nf1 in myogenic cells during postnatal muscle growth required for metabolic and proteostatic homeostasis. Furthermore, Nf1 deficiency in muscle drives cross-tissue communication and mobilization of lipid reserves.

Indexed as

Neurofibromatosis 1AnimalsHomeostasisHumansMiceMuscle DevelopmentMusclesNeurofibromin 1Neurofibromin 1AMPKMuscle atrophyMuscle fibre typeMuscle metabolismMyopathyNeurofibromatosis / NF1

Identifiers

PMID33078583
PMCPMC7749575
OpenAlexW3093039898

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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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 Socratic graph.