ReviewThe international journal of biochemistry & cell biology2013
Molecular mechanisms of muscle atrophy in myotonic dystrophies.
Review in The international journal of biochemistry & cell biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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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
31 citing papers in PubMed.
- Reduced Muscular Carnosine in Proximal Myotonic Myopathy-A PilotAnnals of clinical and translational neurology · 2026Article
- Myotonic dystrophies: an update on clinical features, molecular mechanisms, management, and gene therapy.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Review
- MBNL splicing factors regulate the microtranscriptome of skeletal muscles.Nucleic acids research · 2024Article
- Muscle MRI as a biomarker of disease activity and progression in myotonic dystrophy type 1: a longitudinal study.Journal of neurology · 2024Observational
- Studying the Effect of MBNL1 and MBNL2 Loss in Skeletal Muscle Regeneration.International journal of molecular sciences · 2024Article
- Cutaneous findings in myotonic dystrophy.JAAD international · 2022Article
- Regulatory Potential of Competing Endogenous RNAs in Myotonic Dystrophies.International journal of molecular sciences · 2021Review
- Overexpression of Staufen1 in DM1 mouse skeletal muscle exacerbates dystrophic and atrophic features.Human molecular genetics · 2020Article
- A CRISPR-Cas13a Based Strategy That Tracks and Degrades Toxic RNA in Myotonic Dystrophy Type 1.Frontiers in genetics · 2020Article
- Correction of RNA-Binding Protein CUGBP1 and GSK3β Signaling as Therapeutic Approach for Congenital and Adult Myotonic Dystrophy Type 1.International journal of molecular sciences · 2019Review
- Correction of Glycogen Synthase Kinase 3β in Myotonic Dystrophy 1 Reduces the Mutant RNA and Improves Postnatal Survival of DMSXL Mice.Molecular and cellular biology · 2019Article
- Chronic exercise mitigates disease mechanisms and improves muscle function in myotonic dystrophy type 1 mice.The Journal of physiology · 2019Article
- MBNL1 alternative splicing isoforms play opposing roles in cancer.Life science alliance · 2018Article
- miR-23b and miR-218 silencing increase Muscleblind-like expression and alleviate myotonic dystrophy phenotypes in mammalian models.Nature communications · 2018Article
- Correction of GSK3β at young age prevents muscle pathology in mice with myotonic dystrophy type 1.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Myotonic Dystrophy and Developmental Regulation of RNA Processing.Comprehensive Physiology · 2018Review
- Deregulation of RNA Metabolism in Microsatellite Expansion Diseases.Advances in neurobiology · 2018Review
- Abnormalities in Skeletal Muscle Myogenesis, Growth, and Regeneration in Myotonic Dystrophy.Frontiers in neurology · 2018Review
- (CCUG)Disease models & mechanisms · 2017Article
- CRISPR/Cas9-Induced (CTG⋅CAG)Molecular therapy : the journal of the American Society of Gene Therapy · 2017Article
Corrections and comments
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Authors and funding
1 author.
Funding
Abstract
Myotonic dystrophy type 1 (DM1) and myotonic dystrophy type 2 (DM2) are multisystemic diseases that primarily affect skeletal muscle, causing myotonia, muscle atrophy, and muscle weakness. DM1 and DM2 pathologies are caused by expansion of CTG and CCTG repeats in non-coding regions of the genes encoding myotonic dystrophy protein kinase (DMPK) and zinc finger protein 9 (ZNF9) respectively. These expansions cause DM pathologies through accumulation of mutant RNAs that alter RNA metabolism in patients' tissues by targeting RNA-binding proteins such as CUG-binding protein 1 (CUGBP1) and Muscle blind-like protein 1 (MBNL1). Despite overwhelming evidence showing the critical role of RNA-binding proteins in DM1 and DM2 pathologies, the downstream pathways by which these RNA-binding proteins cause muscle wasting and muscle weakness are not well understood. This review discusses the molecular pathways by which DM1 and DM2 mutations might cause muscle atrophy and describes progress toward the development of therapeutic interventions for muscle wasting and weakness in DM1 and DM2. This article is part of a Directed Issue entitled: Molecular basis of muscle wasting.
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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.