ArticleProceedings of the National Academy of Sciences of the United States of America2006
MyoD expression restores defective myogenic differentiation of human mesoangioblasts from inclusion-body myositis muscle.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 71 citations in OpenAlex.
- Ageing-Associated Dysregulation of Myogenic Differentiation in Inclusion Body Myositis.Journal of cachexia, sarcopenia and muscle · 2026Review
- Approach to Functions ofInternational journal of molecular sciences · 2023Review
- Serum-Circulating microRNAs in Sporadic Inclusion Body Myositis.International journal of molecular sciences · 2023Article
- Frizzled related protein deficiency impairs muscle strength, gait and calpain 3 levels.Orphanet journal of rare diseases · 2020Article
- Muscle Microbiopsy to Delineate Stem Cell Involvement in Young Patients: A Novel Approach for Children With Cerebral Palsy.Frontiers in physiology · 2020Article
- The effect of type 2 diabetes mellitus and obesity on muscle progenitor cell function.Stem cell research & therapy · 2019Review
- Coding Cell Identity of Human Skeletal Muscle Progenitor Cells Using Cell Surface Markers: Current Status and Remaining Challenges for Characterization and Isolation.Frontiers in cell and developmental biology · 2019Review
- Mesenchymal Stem Cells in the Musculoskeletal System: From Animal Models to Human Tissue Regeneration?Stem cell reviews and reports · 2018Review
- Reversible immortalisation enables genetic correction of human muscle progenitors and engineering of next-generation human artificial chromosomes for Duchenne muscular dystrophy.EMBO molecular medicine · 2018Article
- Localization and Expression of Nuclear Factor of Activated T-Cells 5 in Myoblasts Exposed to Pro-inflammatory Cytokines or Hyperosmolar Stress and in Biopsies from Myositis Patients.Frontiers in physiology · 2018Article
- Immune and myodegenerative pathomechanisms in inclusion body myositis.Annals of clinical and translational neurology · 2017Review
- Muscle Tissue Engineering Using Gingival Mesenchymal Stem Cells Encapsulated in Alginate Hydrogels Containing Multiple Growth Factors.Annals of biomedical engineering · 2016Article
- Endothelial sphingosine kinase/SPNS2 axis is critical for vessel-like formation by human mesoangioblasts.Journal of molecular medicine (Berlin, Germany) · 2015Article
- Emerging therapeutic options for sporadic inclusion body myositis.Therapeutics and clinical risk management · 2015Review
- A Genome-Wide mRNA Screen and Functional Analysis Reveal FOXO3 as a Candidate Gene for Chicken Growth.PloS one · 2015Article
- Biocompatible tissue scaffold compliance promotes salivary gland morphogenesis and differentiation.Tissue engineering. Part A · 2014Article
- The role of satellite cells in muscle hypertrophy.Journal of muscle research and cell motility · 2014Review
- Emerging gene editing strategies for Duchenne muscular dystrophy targeting stem cells.Frontiers in physiology · 2014Review
- Sources for skeletal muscle repair: from satellite cells to reprogramming.Journal of cachexia, sarcopenia and muscle · 2013Article
- Satellite cells and the muscle stem cell niche.Physiological reviews · 2013Review
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 2 countries.
Funding
Abstract
Inflammatory myopathies (IM) are acquired diseases of skeletal muscle comprising dermatomyositis (DM), polymyositis (PM), and inclusion-body myositis (IBM). Immunosuppressive therapies, usually beneficial for DM and PM, are poorly effective in IBM. We report the isolation and characterization of mesoangioblasts, vessel-associated stem cells, from diagnostic muscle biopsies of IM. The number of cells isolated, proliferation rate and lifespan, markers expression, and ability to differentiate into smooth muscle do not differ among normal and IM mesoangioblasts. At variance with normal, DM and PM mesoangioblasts, cells isolated from IBM, fail to differentiate into skeletal myotubes. These data correlate with lack in connective tissue of IBM muscle of alkaline phosphatase (ALP)-positive cells, conversely dramatically increased in PM and DM. A myogenic inhibitory basic helix-loop-helix factor B3 is highly expressed in IBM mesoangioblasts. Indeed, silencing this gene or overexpressing MyoD rescues the myogenic defect of IBM mesoangioblasts, opening novel cell-based therapeutic strategies for this crippling disorder.
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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.