ArticleEuropean journal of histochemistry : EJH2014
Premature senescence in primary muscle cultures of myotonic dystrophy type 2 is not associated with p16 induction.
Article in European journal of histochemistry : EJH, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 33 citations in OpenAlex.
- Impaired Myogenic Differentiation Is a Shared Feature Across Genetic Myopathies.International journal of molecular sciences · 2026Review
- New Horizons in Myotonic Dystrophy Type 1: Cellular Senescence as a Therapeutic Target.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- Mortality Trends and Causes of Death in Myotonic Dystrophy Type 1 Patients From the UK Clinical Practice Research Datalink.Muscle & nerve · 2025Article
- Article
- Clearance of defective muscle stem cells by senolytics restores myogenesis in myotonic dystrophy type 1.Nature communications · 2023Article
- Senescence plays a role in myotonic dystrophy type 1.JCI insight · 2022Article
- Targeting Myotonic Dystrophy Type 1 with Metformin.International journal of molecular sciences · 2022Review
- Cellular Senescence and Aging in Myotonic Dystrophy.International journal of molecular sciences · 2022Review
- Expanded CUG Repeat RNA Induces Premature Senescence in Myotonic Dystrophy Model Cells.Frontiers in genetics · 2022Article
- Myogenic Potential of Extracellular Matrix Derived from Decellularized Bovine Pericardium.International journal of molecular sciences · 2021Article
- Nanomedicine for Gene Delivery and Drug Repurposing in the Treatment of Muscular Dystrophies.Pharmaceutics · 2021Review
- Skeletal muscle regeneration in facioscapulohumeral muscular dystrophy is correlated with pathological severity.Human molecular genetics · 2020Article
- Impaired Regeneration in Dystrophic Muscle-New Target for Therapy.Frontiers in molecular neuroscience · 2020Article
- Cored in the act: the use of models to understand core myopathies.Disease models & mechanisms · 2019Review
- Recovery in the Myogenic Program of Congenital Myotonic Dystrophy Myoblasts after Excision of the Expanded (CTG)International journal of molecular sciences · 2019Article
- Myotonic Dystrophy and Developmental Regulation of RNA Processing.Comprehensive Physiology · 2018Review
- Myotonic Dystrophy-A Progeroid Disease?Frontiers in neurology · 2018Article
- Abnormalities in Skeletal Muscle Myogenesis, Growth, and Regeneration in Myotonic Dystrophy.Frontiers in neurology · 2018Review
- Myotonic dystrophy type 2 and modifier genes: an update on clinical and pathomolecular aspects.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2017Review
- Immortalized human myotonic dystrophy muscle cell lines to assess therapeutic compounds.Disease models & mechanisms · 2017Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myotonic dystrophy type 1 (DM1) and type 2 (DM2) are multisystemic disorders linked to two different genetic loci and characterized by several features including myotonia, muscle weakness and atrophy, cardiac dysfunctions, cataracts and insulin-resistance. In both forms, expanded nucleotide sequences cause the accumulation of mutant transcripts in the nucleus deregulating the activity of some RNAbinding proteins and providing an explanation for the multisystemic phenotype of DM patients. However this pathogenetic mechanism does not explain some histopathological features of DM skeletal muscle like muscle atrophy. It has been observed that DM muscle shares similarities with the ageing muscle, where the progressive muscle weakness and atrophy is accompanied by a lower regenerative capacity possibly due to the failure in satellite cells activation. The aim of our study is to investigate if DM2 satellite cell derived myoblasts exhibit a premature senescence as reported for DM1 and if alterations in their proliferation potential and differentiation capabilities might contribute to some of the histopathological features observed in DM2 muscles. Our results indicate that DM myoblasts have lower proliferative capability than control myoblasts and reach in vitro senescence earlier than controls. Differentely from DM1, the p16 pathway is not responsible for the premature growth arrest observed in DM2 myoblasts which stop dividing with telomeres shorter than controls. During in vitro senescence, a progressive decrease in fusion index is observable in both DM and control myotubes with no significant differences between groups. Moreover, myotubes obtained from senescent myoblasts appear to be smaller than those from young myoblasts. Taken together, our data indicate a possible role of DM2 premature myoblast senescence in skeletal muscle histopathological alterations i.e., dystrophic changes and type 2 fibre atrophy.
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