Evidence map›Paper›PMID 39396990›Full record

ArticleSkeletal muscle2024

Exercise, disease state and sex influence the beneficial effects of Fn14-depletion on survival and muscle pathology in the SOD1

Gareth Hazell, Eve McCallion, Nina Ahlskog, Emma R Sutton, Magnus Okoh, Emad I H Shaqoura, Joseph M Hoolachan, Taylor Scaife, Sara Iqbal, Amarjit Bhomra and 5 more

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In one paragraph

Article in Skeletal muscle, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Article
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

15 authors.

Gareth HazellDepartment of Physiology, Anatomy and Genetics, University of Oxford, Oxford, UK.
Eve McCallionSchool of Medicine, Keele University, Staffordshire, UK.
Nina AhlskogDepartment of Physiology, Anatomy and Genetics, University of Oxford, Oxford, UK.
Emma R SuttonSchool of Medicine, Keele University, Staffordshire, UK.
Magnus OkohSchool of Medicine, Keele University, Staffordshire, UK.
Emad I H ShaqouraSchool of Medicine, Keele University, Staffordshire, UK.
Joseph M HoolachanSchool of Medicine, Keele University, Staffordshire, UK.
Taylor ScaifeSchool of Life Sciences, Keele University, Staffordshire, UK.
Sara IqbalSchool of Life Sciences, Keele University, Staffordshire, UK.
Amarjit BhomraDepartment of Physiology, Anatomy and Genetics, University of Oxford, Oxford, UK.
Anna J KordalaDepartment of Physiology, Anatomy and Genetics, University of Oxford, Oxford, UK.
Frederique ScampsINM, Univ Montpellier, INSERM, Montpellier, France.
Cedric RaoulINM, Univ Montpellier, INSERM, Montpellier, France.
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.

Funding

Academy of Medical Sciences SBF006/1162Medical Research Council MR/Y003640/1Muscular Dystrophy UK 18GRO-PS48-0114
6 · The paper itself

Abstract

backgroundAmyotrophic lateral sclerosis (ALS) is a devastating and incurable neurodegenerative disease. Accumulating evidence strongly suggests that intrinsic muscle defects exist and contribute to disease progression, including imbalances in whole-body metabolic homeostasis. We have previously reported that tumour necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) and fibroblast growth factor inducible 14 (Fn14) are significantly upregulated in skeletal muscle of the SOD1

methodsWe thus investigated the contribution of Fn14 to disease phenotypes in the SOD1

resultsHere, we firstly confirm that the TWEAK/Fn14 pathway is dysregulated in skeletal muscle of SOD1

conclusionsOur study provides further insights on the different roles of the TWEAK/Fn14 pathway in pathological skeletal muscle and how they can be influenced by age, disease, sex and exercise. This is particularly relevant in the ALS field, where combinatorial therapies that include exercise regimens are currently being explored. As such, a better understanding and consideration of the interactions between treatments, muscle metabolism, sex and exercise will be of importance in future studies.

Indexed as

Amyotrophic Lateral SclerosisDisease Models, AnimalMice, TransgenicMuscle, SkeletalTWEAK ReceptorAnimalsCytokine TWEAKFemaleMaleMiceMice, Inbred C57BLMice, KnockoutPhysical Conditioning, AnimalSuperoxide Dismutase-1Cytokine TWEAKSuperoxide Dismutase-1Tnfrsf12a protein, mouseTnfsf12 protein, mouseTWEAK ReceptorAmyotrophic lateral sclerosisExerciseFn14MetabolismSexSkeletal muscleTWEAK

Identifiers

PMID39396990
PMCPMC11472643

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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.