ArticleJournal of neurochemistry2010
In AbetaPP-overexpressing cultured human muscle fibers proteasome inhibition enhances phosphorylation of AbetaPP751 and GSK3beta activation: effects mitigated by lithium and apparently relevant to sporadic inclusion-body myositis.
Article in Journal of neurochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 39 citations in OpenAlex.
- Inclusion body myositis, viral infections, and TDP-43: a narrative review.Clinical and experimental medicine · 2024Review
- Sporadic Inclusion Body Myositis at the Crossroads between Muscle Degeneration, Inflammation, and Aging.International journal of molecular sciences · 2024Review
- Updates on the Immunopathology in Idiopathic Inflammatory Myopathies.Current rheumatology reports · 2021Review
- Cell-Clearing Systems Bridging Repeat Expansion Proteotoxicity and Neuromuscular Junction Alterations in ALS and SBMA.International journal of molecular sciences · 2020Review
- Promiscuous Roles of Autophagy and Proteasome in Neurodegenerative Proteinopathies.International journal of molecular sciences · 2020Review
- Article
- Clinical, Histological, and Immunohistochemical Findings in Inclusion Body Myositis.BioMed research international · 2018Article
- Immune and myodegenerative pathomechanisms in inclusion body myositis.Annals of clinical and translational neurology · 2017Review
- Compartment-dependent mitochondrial alterations in experimental ALS, the effects of mitophagy and mitochondriogenesis.Frontiers in cellular neuroscience · 2015Article
- Emerging therapeutic options for sporadic inclusion body myositis.Therapeutics and clinical risk management · 2015Review
- Aberrant cell cycle reentry in human and experimental inclusion body myositis and polymyositis.Human molecular genetics · 2014Article
- Phosphorylation of NBR1 by GSK3 modulates protein aggregation.Autophagy · 2014Article
- Lithium chloride attenuates cell death in oculopharyngeal muscular dystrophy by perturbing Wnt/β-catenin pathway.Cell death & disease · 2013Article
- Differential features of muscle fiber atrophy in osteoporosis and osteoarthritis.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2013Article
- Aggravation effect of isoflurane on Aβ(25-35)-induced apoptosis and tau hyperphosphorylation in PC12 cells.Cellular and molecular neurobiology · 2012Article
- GSK-3 in Neurodegenerative Diseases.International journal of Alzheimer's disease · 2011Article
- Novel therapeutic approaches for inclusion body myositis.Current opinion in rheumatology · 2010Review
- Impaired autophagy in sporadic inclusion-body myositis and in endoplasmic reticulum stress-provoked cultured human muscle fibers.The American journal of pathology · 2010Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Muscle fiber degeneration in sporadic inclusion-body myositis (s-IBM) is characterized by accumulation of multiprotein aggregates, including aggregated amyloid-beta (Abeta)-precursor protein 751 (AbetaPP751), Abeta, phosphorylated tau, and other 'Alzheimer-characteristic' proteins. Proteasome inhibition is an important component of the s-IBM pathogenesis. In brains of Alzheimer's disease (AD) patients and AD transgenic-mouse models, phosphorylation of neuronal AbetaPP695 (p-AbetaPP) on Thr668 (equivalent to T724 of AbetaPP751) is considered detrimental because it increases generation of cytotoxic Abeta and induces tau phosphorylation. Activated glycogen synthase kinase3beta (GSK3beta) is involved in phosphorylation of both AbetaPP and tau. Lithium, an inhibitor of GSK3beta, was reported to reduce levels of both the total AbetaPP and p-AbetaPP in AD animal models. In relation to s-IBM, we now show for the first time that (1) In AbetaPP-overexpressing cultured human muscle fibers (human muscle culture IBM model: (a) proteasome inhibition significantly increases GSK3beta activity and AbetaPP phosphorylation, (b) treatment with lithium decreases (i) phosphorylated-AbetaPP, (ii) total amount of AbetaPP, (iii) Abeta oligomers, and (iv) GSK3beta activity; and (c) lithium improves proteasome function. (2) In biopsied s-IBM muscle fibers, GSK3beta is significantly activated and AbetaPP is phosphorylated on Thr724. Accordingly, treatment with lithium, or other GSK3beta inhibitors, might benefit s-IBM patients.
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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.