ArticleNeurobiology of disease2012
Foxo/atrogin induction in human and experimental myositis.
Article in Neurobiology of disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. 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, 16 citations in OpenAlex.
- Effects and mechanisms of APP and its cleavage product Aβ in the comorbidity of sarcopenia and Alzheimer's disease.Frontiers in aging neuroscience · 2024Review
- Inclusion Body Myositis and Neoplasia: A Narrative Review.International journal of molecular sciences · 2022Review
- Elucidating the Possible Role of FoxO in Depression.Neurochemical research · 2021Review
- The Functional Roles of RNAs Cargoes Released by Neutrophil-Derived Exosomes in Dermatomyositis.Frontiers in pharmacology · 2021Article
- Ongoing developments in sporadic inclusion body myositis.Current rheumatology reports · 2014Review
- Skeletal muscle atrophy and the E3 ubiquitin ligases MuRF1 and MAFbx/atrogin-1.American journal of physiology. Endocrinology and metabolism · 2014Review
- Effects of short-term endurance exercise training on acute doxorubicin-induced FoxO transcription in cardiac and skeletal muscle.Journal of applied physiology (Bethesda, Md. : 1985) · 2014Article
- Aberrant cell cycle reentry in human and experimental inclusion body myositis and polymyositis.Human molecular genetics · 2014Article
- The injury-induced myokine insulin-like 6 is protective in experimental autoimmune myositis.Skeletal muscle · 2014Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
Skeletal muscle atrophy can occur rapidly in various fasting, cancerous, systemic inflammatory, deranged metabolic or neurogenic states. The ubiquitin ligase Atrogin-1 (MAFbx) is induced in animal models of these conditions, causing excessive myoprotein degradation. It is unknown if Atrogin upregulation also occurs in acquired human myositis. Intracellular β-amyloid (Aβi), phosphorylated neurofilaments, scattered infiltrates and atrophy involving selective muscle groups characterize human sporadic Inclusion Body Myositis (sIBM). In Polymyositis (PM), inflammation is more pronounced and atrophy is symmetric and proximal. IBM and PM share various inflammatory markers. We found that forkhead family transcription factor Foxo3A is directed to the nucleus and Atrogin-1 transcript is increased in both conditions. Expression of Aβ in transgenic mice and differentiated C2C12 myotubes was sufficient to upregulate Atrogin-1 mRNA and cause atrophy. Aβi reduces levels of p-Akt and downstream p-Foxo3A, resulting in Foxo3A translocation and Atrogin-1 induction. In a mouse model of autoimmune myositis, cellular inflammation alone was associated with similar Foxo3A and Atrogin changes. Thus, either Aβi accumulation or cellular immune stimulation may independently drive muscle atrophy in sIBM and PM, respectively, through pathways converging on Foxo and Atrogin-1. In sIBM it is additionally possible that both mechanisms synergize.
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Registered trials
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.