ArticleDisease models & mechanisms2015
Increased autophagy and apoptosis contribute to muscle atrophy in a myotonic dystrophy type 1 Drosophila model.
Article in Disease models & mechanisms, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 70 citations in OpenAlex.
- Oxidative stress, aging, metabolism, SIRT1, and the gut microbiota: the neurocardiac basis of cognitive loss.Medical gas research · 2027Review
- Impaired Myogenic Differentiation Is a Shared Feature Across Genetic Myopathies.International journal of molecular sciences · 2026Review
- Oleic Acid Levels in HSAInternational journal of molecular sciences · 2026Article
- dMyc suppresses CTG-induced cytotoxicity in the Drosophila model of DM1 by reducing autophagy and cell death.Cell death discovery · 2026Article
- Emerging roles of microRNAs and other non-coding transcriptome in muscular dystrophies.Inflammation and regeneration · 2026Review
- Disruptions of cell signaling pathways in myotonic dystrophy type 1 skeletal muscle, their pathogenic impact, and potential for combinatorial therapeutics.The Journal of biological chemistry · 2026Review
- Convergent innate immune and regulated cell-death pathways in selected myopathies.Frontiers in immunology · 2026Review
- miR-107 repressesMolecular therapy. Nucleic acids · 2025Article
- Autophagy in Muscle Regeneration: Mechanisms, Targets, and Therapeutic Perspective.International journal of molecular sciences · 2024Review
- Review
- Therapeutic potential of oleic acid supplementation in myotonic dystrophy muscle cell models.Biological research · 2024Article
- Advancing cancer cachexia diagnosis with -omics technology and exercise as molecular medicine.Sports medicine and health science · 2024Review
- Neuroprotective properties of queen bee acid by autophagy induction.Cell biology and toxicology · 2023Article
- CRISPR-Cas9 editing of a TNPO3 mutation in a muscle cell model of limb-girdle muscular dystrophy type D2.Molecular therapy. Nucleic acids · 2023Article
- Senescence plays a role in myotonic dystrophy type 1.JCI insight · 2022Article
- Article
- Partners in crime: Proteins implicated in RNA repeat expansion diseases.Wiley interdisciplinary reviews. RNA · 2022Review
- Deciphering the Complex Molecular Pathogenesis of Myotonic Dystrophy Type 1 through Omics Studies.International journal of molecular sciences · 2022Review
- Identification of DAPK1 as an autophagy-related biomarker for myotonic dystrophy type 1.Frontiers in genetics · 2022Article
- Unravelling the potential neuroprotective facets of erythropoietin for the treatment of Alzheimer's disease.Metabolic brain disease · 2022Review
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Muscle mass wasting is one of the most debilitating symptoms of myotonic dystrophy type 1 (DM1) disease, ultimately leading to immobility, respiratory defects, dysarthria, dysphagia and death in advanced stages of the disease. In order to study the molecular mechanisms leading to the degenerative loss of adult muscle tissue in DM1, we generated an inducible Drosophila model of expanded CTG trinucleotide repeat toxicity that resembles an adult-onset form of the disease. Heat-shock induced expression of 480 CUG repeats in adult flies resulted in a reduction in the area of the indirect flight muscles. In these model flies, reduction of muscle area was concomitant with increased apoptosis and autophagy. Inhibition of apoptosis or autophagy mediated by the overexpression of DIAP1, mTOR (also known as Tor) or muscleblind, or by RNA interference (RNAi)-mediated silencing of autophagy regulatory genes, achieved a rescue of the muscle-loss phenotype. In fact, mTOR overexpression rescued muscle size to a size comparable to that in control flies. These results were validated in skeletal muscle biopsies from DM1 patients in which we found downregulated autophagy and apoptosis repressor genes, and also in DM1 myoblasts where we found increased autophagy. These findings provide new insights into the signaling pathways involved in DM1 disease pathogenesis.
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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.