Evidence map›Paper›PMID 35902978›Full record

ArticleSkeletal muscle2022

Dysregulation of Tweak and Fn14 in skeletal muscle of spinal muscular atrophy mice.

Katharina E Meijboom, Emma R Sutton, Eve McCallion, Emily McFall, Daniel Anthony, Benjamin Edwards, Sabrina Kubinski, Ines Tapken, Ines Bünermann, Gareth Hazell and 6 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Skeletal muscle, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

10 citing papers in PubMed, 10 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

16 authors at 7 institutions in 4 countries.

Katharina E MeijboomDepartment of Physiology, Anatomy and Genetics, University of Oxford, Oxford, UK.
Emma R SuttonSchool of Medicine, Keele University, Staffordshire, UK.
Eve McCallionSchool of Medicine, Keele University, Staffordshire, UK.
Emily McFallRegenerative Medicine Program and Department of Cellular and Molecular Medicine, Ottawa Hospital Research Institute and University of Ottawa, Ottawa, Canada.
Daniel AnthonyDepartment of Pharmacology, University of Oxford, Oxford, UK.
Benjamin EdwardsDepartment of Physiology, Anatomy and Genetics, University of Oxford, Oxford, UK.
Sabrina KubinskiCenter for Systems Neuroscience and Institute of Neuroanatomy and Cell Biology, Hannover Medical School, Hannover, Germany.
Ines TapkenCenter for Systems Neuroscience and Institute of Neuroanatomy and Cell Biology, Hannover Medical School, Hannover, Germany.
Ines BünermannSMATHERIA - Non-Profit Biomedical Research Institute, Hannover, Germany.
Gareth HazellDepartment of Physiology, Anatomy and Genetics, University of Oxford, Oxford, UK.
Nina AhlskogDepartment of Physiology, Anatomy and Genetics, University of Oxford, Oxford, UK.
Peter ClausCenter for Systems Neuroscience and Institute of Neuroanatomy and Cell Biology, Hannover Medical School, Hannover, Germany.
Kay E DaviesDepartment of Physiology, Anatomy and Genetics, University of Oxford, Oxford, UK.
Rashmi KotharyRegenerative Medicine Program and Department of Cellular and Molecular Medicine, Ottawa Hospital Research Institute and University of Ottawa, Ottawa, Canada.
Matthew J A WoodDepartment of Physiology, Anatomy and Genetics, University of Oxford, Oxford, UK.
Melissa BowermanDepartment of Physiology, Anatomy and Genetics, University of Oxford, Oxford, UK. m.bowerman@keele.ac.uk.ORCID 0000-0002-3579-6403
University of Oxford · GBMedizinische Hochschule Hannover · DEKeele University · GBUniversity of Ottawa · CAResearch Institute for Philosophy Hannover · DERobert Jones and Agnes Hunt Orthopaedic Hospital · GBUniversity of Massachusetts Chan Medical School · US

Funding

Academy of Medical Sciences SBF006/1162CIHR
6 · The paper itself

Abstract

backgroundSpinal muscular atrophy (SMA) is a childhood neuromuscular disorder caused by depletion of the survival motor neuron (SMN) protein. SMA is characterized by the selective death of spinal cord motor neurons, leading to progressive muscle wasting. Loss of skeletal muscle in SMA is a combination of denervation-induced muscle atrophy and intrinsic muscle pathologies. Elucidation of the pathways involved is essential to identify the key molecules that contribute to and sustain muscle pathology. The tumor necrosis factor-like weak inducer of apoptosis (TWEAK)/TNF receptor superfamily member fibroblast growth factor-inducible 14 (Fn14) pathway has been shown to play a critical role in the regulation of denervation-induced muscle atrophy as well as muscle proliferation, differentiation, and metabolism in adults. However, it is not clear whether this pathway would be important in highly dynamic and developing muscle.

methodsWe thus investigated the potential role of the TWEAK/Fn14 pathway in SMA muscle pathology, using the severe Taiwanese Smn

resultsHere, we report significantly dysregulated expression of Tweak, Fn14, and previously proposed downstream effectors during disease progression in skeletal muscle of the two SMA mouse models. In addition, siRNA-mediated Smn knockdown in C2C12 myoblasts suggests a genetic interaction between Smn and the TWEAK/Fn14 pathway. Further analyses of SMA, Tweak

conclusionsOur study provides mechanistic insights into potential molecular players that contribute to muscle pathology in SMA and into likely differential responses of the TWEAK/Fn14 pathway in developing muscle.

Indexed as

Muscular Atrophy, SpinalReceptors, Tumor Necrosis FactorAnimalsCytokine TWEAKDisease Models, AnimalMiceMuscle, SkeletalMuscular AtrophyRNA, Small InterferingTranscription FactorsTWEAK ReceptorCytokine TWEAKReceptors, Tumor Necrosis FactorRNA, Small InterferingTnfrsf12a protein, mouseTnfsf12 protein, mouseTranscription FactorsTWEAK ReceptorAtrophyDenervationFn14Glucose metabolismSkeletal muscleSmnSpinal muscular atrophySurvival motor neuronTweak

Identifiers

PMID35902978
PMCPMC9331072
OpenAlexW4288084246

What OpenQuestion holds

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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.