ArticleJournal of immunology (Baltimore, Md. : 1950)2011
Osteopontin-stimulated expression of matrix metalloproteinase-9 causes cardiomyopathy in the mdx model of Duchenne muscular dystrophy.
Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 66 citations in OpenAlex.
- Molecular Mechanisms and Therapeutic Strategies in Heart Failure Due to Dystrophin Deficiency: A Comprehensive Review.Reviews in cardiovascular medicine · 2026Review
- Characterization of a humanized mouse model of Duchenne muscular dystrophy to support the development of genetic medicines.Disease models & mechanisms · 2025Article
- Osteopontin regulates right ventricular failure through integrin ανβ3/PERK/CHOP-dependent inflammatory and apoptotic pathways.Frontiers in immunology · 2025Article
- Review
- Osteopontin in Pulmonary Hypertension.Biomedicines · 2023Review
- COVID-19 Mimics Pulmonary Dysfunction in Muscular Dystrophy as a Post-Acute Syndrome in Patients.International journal of molecular sciences · 2022Review
- Next-Generation SINE Compound KPT-8602 Ameliorates Dystrophic Pathology in Zebrafish and Mouse Models of DMD.Biomedicines · 2022Article
- Clinical and Molecular Implications of Osteopontin in Heart Failure.Current issues in molecular biology · 2022Review
- Single-cell and spatial RNA sequencing identify perturbators of microglial functions with aging.Nature aging · 2022Article
- Lysosomal Function Impacts the Skeletal Muscle Extracellular Matrix.Journal of developmental biology · 2021Article
- Cardiomyocyte-produced miR-339-5p mediates pathology in Duchenne muscular dystrophy cardiomyopathy.Human molecular genetics · 2021Article
- Development of outcome measures according to dystrophic phenotypes in canine X-linked muscular dystrophy in Japan.Experimental animals · 2021Article
- Osteopontin in Cardiovascular Diseases.Biomolecules · 2021Review
- Cardiac fibrosis.Cardiovascular research · 2021Review
- Dystrophin Deficiency Causes Progressive Depletion of Cardiovascular Progenitor Cells in the Heart.International journal of molecular sciences · 2021Article
- Role of the Renin-Angiotensin-Aldosterone System in Dystrophin-Deficient Cardiomyopathy.International journal of molecular sciences · 2020Review
- Prostatic osteopontin expression is associated with symptomatic benign prostatic hyperplasia.The Prostate · 2020Article
- Osteopontin and Integrin Mediated Modulation of Post-Synapses in HIV Envelope Glycoprotein Exposed Hippocampal Neurons.Brain sciences · 2020Article
- Regulation of Myocardial Extracellular Matrix Dynamic Changes in Myocardial Infarction and Postinfarct Remodeling.Current cardiology reviews · 2020Review
- Spp1 (osteopontin) promotes TGFβ processing in fibroblasts of dystrophin-deficient muscles through matrix metalloproteinases.Human molecular genetics · 2019Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Duchenne muscular dystrophy (DMD), caused by mutations in the dystrophin gene, is a common and lethal form of muscular dystrophy. With progressive disease, most patients succumb to death from respiratory or heart failure, or both. However, the mechanisms, especially those governing cardiac inflammation and fibrosis in DMD, remain less understood. Matrix metalloproteinase (MMPs) are a group of extracellular matrix proteases involved in tissue remodeling in both physiologic and pathophysiologic conditions. Previous studies have shown that MMP-9 exacerbates myopathy in dystrophin-deficient mdx mice. However, the role and the mechanisms of action of MMP-9 in cardiac tissue and the biochemical mechanisms leading to increased levels of MMP-9 in mdx mice remain unknown. Our results demonstrate that the levels of MMP-9 are increased in the heart of mdx mice. Genetic ablation of MMP-9 attenuated cardiac injury, left ventricle dilation, and fibrosis in 1-y-old mdx mice. Echocardiography measurements showed improved heart function in Mmp9-deficient mdx mice. Deletion of the Mmp9 gene diminished the activation of ERK1/2 and Akt kinase in the heart of mdx mice. Ablation of MMP-9 also suppressed the expression of MMP-3 and MMP-12 in the heart of mdx mice. Finally, our experiments have revealed that osteopontin, an important immunomodulator, contributes to the increased amounts of MMP-9 in cardiac and skeletal muscle of mdx mice. This study provides a novel mechanism for development of cardiac dysfunction and suggests that MMP-9 and OPN are important therapeutic targets to mitigating cardiac abnormalities in patients with DMD.
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