Exercise, disease state and sex influence the beneficial effects of Fn14-depletion on survival and muscle pathology in the SOD1
Amyotrophic lateral sclerosis
Exercise
Fn14
Metabolism
Sex
Skeletal muscle
TWEAK
Journal
Skeletal muscle
ISSN: 2044-5040
Titre abrégé: Skelet Muscle
Pays: England
ID NLM: 101561193
Informations de publication
Date de publication:
14 Oct 2024
14 Oct 2024
Historique:
received:
05
07
2024
accepted:
04
10
2024
medline:
14
10
2024
pubmed:
14
10
2024
entrez:
13
10
2024
Statut:
epublish
Résumé
Amyotrophic 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 We thus investigated the contribution of Fn14 to disease phenotypes in the SOD1 Here, we firstly confirm that the TWEAK/Fn14 pathway is dysregulated in skeletal muscle of SOD1 Our 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.
Sections du résumé
BACKGROUND
BACKGROUND
Amyotrophic 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
METHODS
METHODS
We thus investigated the contribution of Fn14 to disease phenotypes in the SOD1
RESULTS
RESULTS
Here, we firstly confirm that the TWEAK/Fn14 pathway is dysregulated in skeletal muscle of SOD1
CONCLUSIONS
CONCLUSIONS
Our 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.
Identifiants
pubmed: 39396990
doi: 10.1186/s13395-024-00356-0
pii: 10.1186/s13395-024-00356-0
doi:
Substances chimiques
TWEAK Receptor
0
Tnfrsf12a protein, mouse
0
Cytokine TWEAK
0
Superoxide Dismutase-1
EC 1.15.1.1
Tnfsf12 protein, mouse
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
23Subventions
Organisme : Academy of Medical Sciences
ID : SBF006/1162
Pays : United Kingdom
Organisme : Academy of Medical Sciences
ID : SBF006/1162
Pays : United Kingdom
Organisme : Medical Research Council
ID : MR/Y003640/1
Pays : United Kingdom
Organisme : Medical Research Council
ID : MR/Y003640/1
Pays : United Kingdom
Organisme : Muscular Dystrophy UK
ID : 18GRO-PS48-0114
Organisme : Muscular Dystrophy UK
ID : 18GRO-PS48-0114
Informations de copyright
© 2024. Crown.
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