Trial reportEuropean journal of histochemistry : EJH2011
Cultured myoblasts from patients affected by myotonic dystrophy type 2 exhibit senescence-related features: ultrastructural evidence.
Trial report in European journal of histochemistry : EJH, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed.
- Article
- Impaired Myogenic Differentiation Is a Shared Feature Across Genetic Myopathies.International journal of molecular sciences · 2026Review
- Local Non-Coding Regulatory Elements in Muscular Dystrophies.International journal of molecular sciences · 2025Review
- Article
- Human Myobundle Platform for Studying the Role of Notch Signaling in Satellite Cell Phenotype and Function.Advanced healthcare materials · 2025Article
- New Horizons in Myotonic Dystrophy Type 1: Cellular Senescence as a Therapeutic Target.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- A Phyto-mycotherapeutic Supplement, NamelyInternational journal of molecular sciences · 2024Article
- Histochemistry for nucleic acid research: 60 years in the European Journal of Histochemistry.European journal of histochemistry : EJH · 2022Review
- Cellular Senescence and Aging in Myotonic Dystrophy.International journal of molecular sciences · 2022Review
- Pathogenic mechanism and modeling of neuroferritinopathy.Cellular and molecular life sciences : CMLS · 2021Review
- Stem Cell Modeling of Neuroferritinopathy Reveals Iron as a Determinant of Senescence and Ferroptosis during Neuronal Aging.Stem cell reports · 2019Article
- Ultrastructural histochemistry in biomedical research: Alive and kicking.European journal of histochemistry : EJH · 2018Article
- Myotonic Dystrophy-A Progeroid Disease?Frontiers in neurology · 2018Article
- 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
- Article
- Myotonic Dystrophy Type 2: An Update on Clinical Aspects, Genetic and Pathomolecular Mechanism.Journal of neuromuscular diseases · 2015Article
- A muscle stem cell for every muscle: variability of satellite cell biology among different muscle groups.Frontiers in aging neuroscience · 2015Review
- Muscle wasting in myotonic dystrophies: a model of premature aging.Frontiers in aging neuroscience · 2015Review
- Premature senescence in primary muscle cultures of myotonic dystrophy type 2 is not associated with p16 induction.European journal of histochemistry : EJH · 2014Article
- RNA Transcription and Maturation in Skeletal Muscle Cells are Similarly Impaired in Myotonic Dystrophy and Sarcopenia: The Ultrastructural Evidence.Frontiers in aging neuroscience · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myotonic dystrophy type 2 (DM2) is an autosomal dominant disorder caused by the expansion of the tetranucleotidic repeat (CCTG)n in the first intron of the Zinc Finger Protein-9 gene. In DM2 tissues, the expanded mutant transcripts accumulate in nuclear focal aggregates where splicing factors are sequestered, thus affecting mRNA processing. Interestingly, the ultrastructural alterations in the splicing machinery observed in the myonuclei of DM2 skeletal muscles are reminiscent of the nuclear changes occurring in age-related muscle atrophy. Here, we investigated in vitro structural and functional features of satellite cell-derived myoblasts from biceps brachii, in the attempt to investigate cell senescence indices in DM2 patients by ultrastructural cytochemistry. We observed that in satellite cell-derived DM2 myoblasts, cell-senescence alterations such as cytoplasmic vacuolization, reduction of the proteosynthetic apparatus, accumulation of heterochromatin and impairment of the pre-mRNA maturation pathways occur earlier than in myoblasts from healthy patients. These results, together with preliminary in vitro observations on the early onset of defective structural features in DM2 myoblast derived-myotubes, suggest that the regeneration capability of DM2 satellite cells may be impaired, thus contributing to the muscular dystrophy in DM2 patients.
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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.