ArticleHuman molecular genetics2011
Elevated levels of active matrix metalloproteinase-9 cause hypertrophy in skeletal muscle of normal and dystrophin-deficient mdx mice.
Article in Human molecular genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 73 citations in OpenAlex.
- Effect of dietary n-3 PUFA supplementation on the muscle transcriptome in older adults.Physiological reports · 2016Trial
- Characterization of a humanized mouse model of Duchenne muscular dystrophy to support the development of genetic medicines.Disease models & mechanisms · 2025Article
- Intermediate Signaling Mechanisms Regulating Human Fetal Membrane Responses to Gram-Positive Bacterial Peptidoglycan.American journal of reproductive immunology (New York, N.Y. : 1989) · 2025Article
- Functional Foods, a Hope to Delay Muscle Dystrophy Progression: A Potential Role for Omega Fatty Acids.Nutrients · 2025Review
- Gene Manipulation of Muscle Phenotype.Advances in experimental medicine and biology · 2025Review
- The roles of miRNAs in adult skeletal muscle satellite cells.Free radical biology & medicine · 2023Review
- Role of Matrix Metalloproteinases in Musculoskeletal Diseases.Biomedicines · 2022Review
- A glitch in the matrix: the pivotal role for extracellular matrix remodeling during muscle hypertrophy.American journal of physiology. Cell physiology · 2022Review
- Myotendinous Junction: Exercise Protocols Can Positively Influence Their Development in Rats.Biomedicines · 2022Article
- RhoA within myofibers controls satellite cell microenvironment to allow hypertrophic growth.iScience · 2022Article
- Actions and interactions of IGF-I and MMPs during muscle regeneration.Seminars in cell & developmental biology · 2021Review
- Polymeric nanoparticles functionalized with muscle-homing peptides for targeted delivery of phosphatase and tensin homolog inhibitor to skeletal muscle.Acta biomaterialia · 2020Article
- Myotendinous junction adaptations to ladder-based resistance training: identification of a new telocyte niche.Scientific reports · 2020Article
- Simultaneous Enrichment Analysis of all Possible Gene-sets: Unifying Self-Contained and Competitive Methods.Briefings in bioinformatics · 2020Review
- Matrix Metalloproteinase 13 from Satellite Cells is Required for Efficient Muscle Growth and Regeneration.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2020Article
- Review
- Fusion-Independent Satellite Cell Communication to Muscle Fibers During Load-Induced Hypertrophy.Function (Oxford, England) · 2020Article
- Spp1 (osteopontin) promotes TGFβ processing in fibroblasts of dystrophin-deficient muscles through matrix metalloproteinases.Human molecular genetics · 2019Article
- Basal lamina remodeling at the skeletal muscle stem cell niche mediates stem cell self-renewal.Nature communications · 2018Article
- Cathepsin K activity controls cardiotoxin-induced skeletal muscle repair in mice.Journal of cachexia, sarcopenia and muscle · 2018Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Matrix metalloproteinases (MMPs) are a group of extracellular proteases involved in tissue remodeling in several physiological and pathophysiological conditions. While increased expression of MMPs (especially MMP-9) has been observed in skeletal muscle in numerous conditions, their physiological significance remains less-well understood. By generating novel skeletal muscle-specific transgenic (Tg) mice expressing constitutively active mutant of MMP-9 (i.e. MMP-9G100L), in this study, we have investigated the effects of elevated levels of MMP-9 on skeletal muscle structure and function in vivo. Tg expression of enzymatically active MMP-9 protein significantly increased skeletal muscle fiber cross-section area, levels of contractile proteins and force production in isometric contractions. MMP-9 stimulated the activation of the Akt signaling pathway in Tg mice. Moreover, expression of active MMP-9 increased the proportion of fast-type fiber in soleus muscle of mice. Overexpression of MMP-9 also considerably reduced the deposition of collagens I and IV in skeletal muscle in vivo. In one-year-old mdx mice (a model for Duchenne muscular dystrophy, DMD), deletion of the Mmp9 gene reduced fiber hypertrophy and phosphorylation of Akt and p38 mitogen-activated protein kinase. Collectively, our study suggests that elevated levels of active MMP-9 protein cause hypertrophy in skeletal muscle and that the modulation of MMP-9 levels may have therapeutic value in various muscular disorders including DMD.
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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.