Cardiomyopathy in the dystrophin/utrophin-deficient mouse model of severe muscular dystrophy is characterized by dysregulation of matrix metalloproteinases
Open accessAbstract
Cardiomyopathy is a significant component in Duchenne muscular dystrophy. Although mdx mice are deficient in dystrophin, they only develop mild indicators of cardiomyopathy before 1year-of-age, making therapeutic investigations using this model lengthy. In contrast, mdx mice also lacking utrophin (utrn(-/-);mdx) show severely reduced cardiac contractile function and histological indicators of cardiomyopathy by 8-10weeks-of-age. Here we demonstrate that utrn(-/-);mdx mice show a similar pattern of cardiac damage to that in dystrophic patients. Matrix metalloproteinases required for ventricular remodeling during the evolution of heart failure are upregulated in utrn(-/-);mdx mice concurrent with the onset of cardiac pathology by 10weeks-of-age. Matrix metalloproteinase activity is further dysregulated due to reduced levels of endogenous tissue inhibitors and co-localizes with fibroblasts and collagen I-containing scars. utrn(-/-);mdx mice are therefore a very useful model for investigating potential cardiac therapies.
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Mice lacking both dystrophin and utrophin show a much more severe phenotype and reduced lifespan.
“a mouse model lacking both dystrophin and utrophin shows a much more severe phenotype, and a reduced lifespan”
From Small and large animal models in cardiac contraction research: advantages and disadvantages (2014) · cites this paper as Delfin, et al., 2011
The mdx mouse model has mild cardiomyopathy, mild limb-skeletal muscle dysfunction, and normal life span, unlike human DMD.
“The mdx (dystrophin deficient) mouse model has a rather mild cardiomyopathy, mild limb-skeletal muscle dysfunction, and a normal life span, in contrast to human counterparts”
From Small and large animal models in cardiac contraction research: advantages and disadvantages (2014) · cites this paper as Delfin, et al., 2011
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- Authors
- Delfín, D. A., Zang, K. E., Schill, K. E., Patel, N. T., Janssen, P. M. L., Raman, S. V., & Rafael-Fortney, J. A.
- Affiliations
- The Ohio State University (US)
- Venue
- Neuromuscular Disorders
- Publisher
- Elsevier BV
- Published
- 2012-11
- Volume
- 22
- Issue
- 11
- Pages
- 1006-1014
- ISSN
- 0960-8966 (ISSN-L)
- PMC
- PMC3484217
- OpenAlex
- W2092556059
- Cited by
- 27
- References
- 50
- Citations by year
- 2026: 2 · 2024: 1 · 2023: 1 · 2022: 3 · 2021: 3 · 2020: 2 · 2019: 1 · 2017: 4 · 2016: 1 · 2015: 1 · 2014: 3 · 2013: 4 · 2012: 1
- FWCI
- 1.16
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Neuromuscular Disorders (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Muscular Dystrophy Association
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiomyopathy and Myosin Studies
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Keywords
- cardiomyopathy, Duchenne muscular dystrophy, dystrophin deficiency, mdx mice, matrix metalloproteinases, tissue inhibitors of metalloproteinases, cardiac remodeling, heart failure, fibroblasts, type I collagen, cardiac contractile function, mouse model
- MeSH terms
- Animals, Disease Models, Animal, Female, Heart Failure, Humans, Male, Mice, Inbred C57BL, Cardiomyopathies, Dystrophin, Mice, Inbred mdx, Mice, Knockout, Muscle, Skeletal, Muscular Dystrophy, Duchenne, Matrix Metalloproteinases, Utrophin, Mice
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