ArticleBMC musculoskeletal disorders2011
The proteasome inhibitor MG132 reduces immobilization-induced skeletal muscle atrophy in mice.
Article in BMC musculoskeletal disorders, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.
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Who cites it
50 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.
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- A holistic approach for severe flexion contracture of bilateral hip, knee, and ankle joints in a neglected patient with prolonged knee-chest positioning on extreme undernourishment: a case report and review of the literature.Journal of medical case reports · 2022Review
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- Proteasome- and Calpain-Mediated Proteolysis, but Not Autophagy, Is Required for Leucine-Induced Protein Synthesis in C2C12 Myotubes.Physiologia · 2021Article
- Control of Skeletal Muscle Atrophy Associated to Cancer or Corticosteroids by Ceramide Kinase.Cancers · 2021Article
- Autophagy triggers CTSD (cathepsin D) maturation and localization inside cells to promote apoptosis.Autophagy · 2021Article
- Breakdown of Filamentous Myofibrils by the UPS-Step by Step.Biomolecules · 2021Review
- Histone Deacetylase 2 Suppresses Skeletal Muscle Atrophy and Senescence via NF-κB Signaling Pathway in Cigarette Smoke-Induced Mice with Emphysema.International journal of chronic obstructive pulmonary disease · 2021Article
- Flavonoids: nutraceutical potential for counteracting muscle atrophy.Food science and biotechnology · 2020Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundSkeletal muscle atrophy is a serious concern for the rehabilitation of patients afflicted by prolonged limb restriction. This debilitating condition is associated with a marked activation of NFκB activity. The ubiquitin-proteasome pathway degrades the NFκB inhibitor IκBα, enabling NFκB to translocate to the nucleus and bind to the target genes that promote muscle atrophy. Although several studies showed that proteasome inhibitors are efficient to reduce atrophy, no studies have demonstrated the ability of these inhibitors to preserve muscle function under catabolic condition.
methodsWe recently developed a new hindlimb immobilization procedure that induces significant skeletal muscle atrophy and used it to show that an inflammatory process characterized by the up-regulation of TNFα, a known activator of the canonical NFκB pathway, is associated with the atrophy. Here, we used this model to investigate the effect of in vivo proteasome inhibition on the muscle integrity by histological approach. TNFα, IL-1, IL-6, MuRF-1 and Atrogin/MAFbx mRNA level were determined by qPCR. Also, a functional measurement of locomotors activity was performed to determine if the treatment can shorten the rehabilitation period following immobilization.
resultsIn the present study, we showed that the proteasome inhibitor MG132 significantly inhibited IκBα degradation thus preventing NFκB activation in vitro. MG132 preserved muscle and myofiber cross-sectional area by downregulating the muscle-specific ubiquitin ligases atrogin-1/MAFbx and MuRF-1 mRNA in vivo. This effect resulted in a diminished rehabilitation period.
conclusionThese finding demonstrate that proteasome inhibitors show potential for the development of pharmacological therapies to prevent muscle atrophy and thus favor muscle rehabilitation.
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