ArticlePloS one2013
Matrix metalloproteinase-9 inhibition improves proliferation and engraftment of myogenic cells in dystrophic muscle of mdx mice.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 73 citations in OpenAlex.
- Matrix metalloproteinases are hallmark early biomarkers and therapeutic targets in FSHD.JCI insight · 2025Article
- Extracellular matrix in skeletal muscle injury and atrophy: mechanisms and therapeutic implications.Journal of orthopaedic translation · 2025Review
- Differential regulation of MMP activity by TGFβ1 in fast- and slow- twitch muscle repair: insights from EDL and soleus muscle-derived myoblasts.Frontiers in cell and developmental biology · 2025Article
- Molecular basis of proteolytic cleavage regulation by the extracellular matrix receptor dystroglycan.Structure (London, England : 1993) · 2024Article
- Matrix metalloproteinase-9 deficiency confers resilience in fibrodysplasia ossificans progressiva in a man and mice.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2024Article
- Role of Matrix Metalloproteinases in Musculoskeletal Diseases.Biomedicines · 2022Review
- Macrophages in Skeletal Muscle Dystrophies, An Entangled Partner.Journal of neuromuscular diseases · 2022Review
- Synthetic polypeptide crotamine: characterization as a myotoxin and as a target of combinatorial peptides.Journal of molecular medicine (Berlin, Germany) · 2022Article
- Implications of notch signaling in duchenne muscular dystrophy.Frontiers in physiology · 2022Review
- Codon Usage Bias and Cluster Analysis of theGenetics research · 2022Article
- The Critical Role of MMP13 in Regulating Tooth Development and Reactionary Dentinogenesis Repair Through the Wnt Signaling Pathway.Frontiers in cell and developmental biology · 2022Article
- Actions and interactions of IGF-I and MMPs during muscle regeneration.Seminars in cell & developmental biology · 2021Review
- Skeletal muscle regeneration with robotic actuation-mediated clearance of neutrophils.Science translational medicine · 2021Article
- Therapeutic aspects of cell signaling and communication in Duchenne muscular dystrophy.Cellular and molecular life sciences : CMLS · 2021Review
- Simultaneous Enrichment Analysis of all Possible Gene-sets: Unifying Self-Contained and Competitive Methods.Briefings in bioinformatics · 2020Review
- Review
- Article
- Comparative study of calcium and calcium-related enzymes with differentiation markers in different ages and muscle types in mdx mice.Histology and histopathology · 2020Article
- Hydrogen Sulfide Alleviates Skeletal Muscle Fibrosis via Attenuating Inflammation and Oxidative Stress.Frontiers in physiology · 2020Article
- Regenerative Repair of Volumetric Muscle Loss Injury is Sensitive to Age.Tissue engineering. Part A · 2020Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Duchenne muscular dystrophy (DMD) caused by loss of cytoskeletal protein dystrophin is a devastating disorder of skeletal muscle. Primary deficiency of dystrophin leads to several secondary pathological changes including fiber degeneration and regeneration, extracellular matrix breakdown, inflammation, and fibrosis. Matrix metalloproteinases (MMPs) are a group of extracellular proteases that are involved in tissue remodeling, inflammation, and development of interstitial fibrosis in many disease states. We have recently reported that the inhibition of MMP-9 improves myopathy and augments myofiber regeneration in mdx mice (a mouse model of DMD). However, the mechanisms by which MMP-9 regulates disease progression in mdx mice remain less understood. In this report, we demonstrate that the inhibition of MMP-9 augments the proliferation of satellite cells in dystrophic muscle. MMP-9 inhibition also causes significant reduction in percentage of M1 macrophages with concomitant increase in the proportion of promyogenic M2 macrophages in mdx mice. Moreover, inhibition of MMP-9 increases the expression of Notch ligands and receptors, and Notch target genes in skeletal muscle of mdx mice. Furthermore, our results show that while MMP-9 inhibition augments the expression of components of canonical Wnt signaling, it reduces the expression of genes whose products are involved in activation of non-canonical Wnt signaling in mdx mice. Finally, the inhibition of MMP-9 was found to dramatically improve the engraftment of transplanted myoblasts in skeletal muscle of mdx mice. Collectively, our study suggests that the inhibition of MMP-9 is a promising approach to stimulate myofiber regeneration and improving engraftment of muscle progenitor cells in dystrophic muscle.
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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.