ArticlePloS one2025
Respiratory pathology in the mdx/utrn -/- mouse: A murine model for Duchenne Muscular Dystrophy (DMD).
Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- AAVcc47-The Yale journal of biology and medicine · 2026Article
- Neuromuscular and neuromechanical assessments of respiratory performance in the mdx mouse model of Duchenne muscular dystrophy across the natural history of disease.Experimental physiology · 2026Article
- PPMO-based exon skipping therapy improves respiratory function in theMolecular therapy. Nucleic acids · 2026Article
- Col6a1 knock-in mice provide a promising pre-clinical model for collagen VI-related dystrophies.Disease models & mechanisms · 2026Article
- Stepping up to inspire in muscular dystrophy.The Journal of physiology · 2025Article
- AAV9 gene therapy to target respiratory insufficiency in the D2.mdx mouse model of duchenne muscular dystrophy.Respiratory physiology & neurobiologyArticle
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Authors and funding
11 authors.
Funding
Abstract
Duchenne muscular dystrophy (DMD) is an X-linked devastating disease caused by a lack of dystrophin which results in progressive muscle weakness. As muscle weakness progresses, respiratory insufficiency and hypoventilation result in significant morbidity and mortality. The most studied DMD mouse model- the mdx mouse- has a milder respiratory phenotype compared to humans, likely due to compensatory overexpression of utrophin. mdx/utrn-/- mice lack both dystrophin and utrophin proteins. These mice have an early onset of muscular dystrophy, severe muscle weakness, and premature death, but the respiratory pathophysiology is unclear. The objective of this study is to characterize the respiratory pathophysiology and histopathology using whole body plethysmography to measure breathing and metabolism, diaphragm muscle functional analysis, histology, and immunohistochemistry. The mdx/utrn-/- mice have significant respiratory and metabolic deficits with respiratory insufficiency and hypoventilation when exposed to hypoxia and hypercarbia as early as 6 weeks of age. They also have significant diaphragmatic weakness and disrupted diaphragmatic structural pathology. The mdx/utrn-/- mice display respiratory dysfunction that mimics the DMD phenotype and therefore can provide a useful model to study the impact of novel therapies on respiratory function for DMD.
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Registered trials
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