ReviewJournal of biomedicine & biotechnology2011
Mammalian models of Duchenne Muscular Dystrophy: pathological characteristics and therapeutic applications.
Review in Journal of biomedicine & biotechnology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
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
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 110 citations in OpenAlex.
- Pooled it
- RNA Therapeutics Targeting Skeletal Muscle: Emerging Antisense and Gene-Modifying Strategies.Biomolecules · 2026Review
- Obestatin: canonical and unexpected functions.Reviews in endocrine & metabolic disorders · 2026Review
- RNA Therapeutics for Duchenne Muscular Dystrophy: Exon Skipping, RNA Editing, and Translational Insights from Genome-Edited Microminipig Models.International journal of molecular sciences · 2026Review
- Anti-Inflammatory and Synaptic Protective Effects of TNF-α Inactivation in the MDX Mouse Model.Current issues in molecular biology · 2026Article
- Detection of Locked Nucleic Acid and 2'-O-Methoxyethyl Gapmers from Mouse Samples Using ELISA.Methods in molecular biology (Clifton, N.J.) · 2026Article
- High mobility group box 1 (HMGB1) is a potential disease biomarker in cell and mouse models of Duchenne muscular dystrophy.Biology open · 2024Article
- Production of Duchenne muscular dystrophy cellular model using CRISPR-Cas9 exon deletion strategy.Molecular and cellular biochemistry · 2024Article
- Dystrophin (International journal of molecular sciences · 2023Article
- A new immunodeficient Duchenne muscular dystrophy rat model to evaluate engraftment after human cell transplantation.Frontiers in physiology · 2023Article
- Sphingosine Phosphate Lyase Is Upregulated in Duchenne Muscular Dystrophy, and Its Inhibition Early in Life Attenuates Inflammation and Dystrophy in Mdx Mice.International journal of molecular sciences · 2022Article
- The role of Nrf2 in acute and chronic muscle injury.Skeletal muscle · 2020Article
- Cardiac lesions in Duchenne muscular dystrophy model rats with out-of-frameJournal of toxicologic pathology · 2020Article
- Optimization of antisense-mediated exon skipping for Duchenne muscular dystrophy.Gene therapy · 2020Review
- miR-146a deficiency does not aggravate muscular dystrophy in mdx mice.Skeletal muscle · 2019Article
- Adipose-Derived Mesenchymal Stem Cells: A Promising Tool in the Treatment of Musculoskeletal Diseases.International journal of molecular sciences · 2019Review
- Targeting angiogenesis in Duchenne muscular dystrophy.Cellular and molecular life sciences : CMLS · 2019Review
- Mutation-Based Therapeutic Strategies for Duchenne Muscular Dystrophy: From Genetic Diagnosis to Therapy.Journal of personalized medicine · 2019Review
- Antisense oligonucleotides for the treatment of cardiomyopathy in Duchenne muscular dystrophy.American journal of translational research · 2019Review
- Photobiomodulation therapy protects skeletal muscle and improves muscular function of mdx mice in a dose-dependent manner through modulation of dystrophin.Lasers in medical science · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Duchenne muscular dystrophy (DMD) is a devastating X-linked muscle disorder characterized by muscle wasting which is caused by mutations in the DMD gene. The DMD gene encodes the sarcolemmal protein dystrophin, and loss of dystrophin causes muscle degeneration and necrosis. Thus far, therapies for this disorder are unavailable. However, various therapeutic trials based on gene therapy, exon skipping, cell therapy, read through therapy, or pharmaceutical agents have been conducted extensively. In the development of therapy as well as elucidation of pathogenesis in DMD, appropriate animal models are needed. Various animal models of DMD have been identified, and mammalian (murine, canine, and feline) models are indispensable for the examination of the mechanisms of pathogenesis and the development of therapies. Here, we review the pathological features of DMD and therapeutic applications, especially of exon skipping using antisense oligonucleotides and gene therapies using viral vectors in murine and canine models of DMD.
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What OpenQuestion holds
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.