ArticlePloS one2012
Impaired adaptive response to mechanical overloading in dystrophic skeletal muscle.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 9 papers.
What it found
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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.
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Who cites it
9 citing papers in PubMed.
- Article
- Absence of Desmin Results in Impaired Adaptive Response to Mechanical Overloading of Skeletal Muscle.Frontiers in cell and developmental biology · 2021Article
- Molecular Mechanisms of Skeletal Muscle Hypertrophy.Journal of neuromuscular diseases · 2021Review
- Effects of the selective inhibition of proteasome caspase-like activity by CLi a derivative of nor-cerpegin in dystrophic mdx mice.PloS one · 2019Article
- Dystrophin restoration therapy improves both the reduced excitability and the force drop induced by lengthening contractions in dystrophic mdx skeletal muscle.Skeletal muscle · 2016Article
- Six homeoproteins and a Iinc-RNA at the fast MYH locus lock fast myofiber terminal phenotype.PLoS genetics · 2014Article
- Autophagy is Impaired in the Tibialis Anterior of Dystrophin Null Mice.PLoS currents · 2013Article
- Loss of cIAP1 attenuates soleus muscle pathology and improves diaphragm function in mdx mice.Human molecular genetics · 2013Article
- Viral-mediated expression of desmin mutants to create mouse models of myofibrillar myopathy.Skeletal muscle · 2013Article
Corrections and comments
- Erratum issuedSakamato, Kei [name corrected to Sakamoto, Kei]
Authors and funding
18 authors.
Funding
Abstract
Dystrophin contributes to force transmission and has a protein-scaffolding role for a variety of signaling complexes in skeletal muscle. In the present study, we tested the hypothesis that the muscle adaptive response following mechanical overloading (ML) would be decreased in MDX dystrophic muscle lacking dystrophin. We found that the gains in muscle maximal force production and fatigue resistance in response to ML were both reduced in MDX mice as compared to healthy mice. MDX muscle also exhibited decreased cellular and molecular muscle remodeling (hypertrophy and promotion of slower/oxidative fiber type) in response to ML, and altered intracellular signalings involved in muscle growth and maintenance (mTOR, myostatin, follistatin, AMPKα1, REDD1, atrogin-1, Bnip3). Moreover, dystrophin rescue via exon skipping restored the adaptive response to ML. Therefore our results demonstrate that the adaptive response in response to ML is impaired in dystrophic MDX muscle, most likely because of the dystrophin crucial role.
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Registered trials
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