ArticleThe Journal of cell biology2007
uPA deficiency exacerbates muscular dystrophy in MDX mice.
Article in The Journal of cell biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 69 citations in OpenAlex.
- Pharmacotherapeutic Approaches to Treatment of Muscular Dystrophies.Biomolecules · 2023Review
- 3-deazaadenosine (3DA) alleviates senescence to promote cellular fitness and cell therapy efficiency in mice.Nature aging · 2022Article
- Myxomavirus Serp-1 Protein Ameliorates Inflammation in a Mouse Model of Duchenne Muscular Dystrophy.Biomedicines · 2022Article
- Macrophages in Skeletal Muscle Dystrophies, An Entangled Partner.Journal of neuromuscular diseases · 2022Review
- Glucose 6-P dehydrogenase delays the onset of frailty by protecting against muscle damage.Journal of cachexia, sarcopenia and muscle · 2021Article
- Mesenchymal stem cells derived from human induced pluripotent stem cells improve the engraftment of myogenic cells by secreting urokinase-type plasminogen activator receptor (uPAR).Stem cell research & therapy · 2021Article
- Plasminogen Activator Inhibitor-1 and Oncogenesis in the Liver Disease.Journal of cellular signaling · 2021Article
- FoxO maintains a genuine muscle stem-cell quiescent state until geriatric age.Nature cell biology · 2020Article
- PAI-1, the Plasminogen System, and Skeletal Muscle.International journal of molecular sciences · 2020Review
- Regulation of fibrosis in muscular dystrophy.Matrix biology : journal of the International Society for Matrix Biology · 2018Review
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- Elastase levels and activity are increased in dystrophic muscle and impair myoblast cell survival, proliferation and differentiation.Scientific reports · 2016Article
- Osteopontin ablation ameliorates muscular dystrophy by shifting macrophages to a pro-regenerative phenotype.The Journal of cell biology · 2016Article
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- Fibrinolysis is essential for fracture repair and prevention of heterotopic ossification.The Journal of clinical investigation · 2015Article
- Age and aerobic training status effects on plasma and skeletal muscle tPA and PAI-1.European journal of applied physiology · 2014Article
- Shared signaling systems in myeloid cell-mediated muscle regeneration.Development (Cambridge, England) · 2014Review
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- Understanding the process of fibrosis in Duchenne muscular dystrophy.BioMed research international · 2014Review
Corrections and comments
- Erratum issuedDíaz, Maria Angels [corrected to Díaz-Ramos, Angels]
Authors and funding
16 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Duchenne muscular dystrophy (DMD) is a fatal and incurable muscle degenerative disorder. We identify a function of the protease urokinase plasminogen activator (uPA) in mdx mice, a mouse model of DMD. The expression of uPA is induced in mdx dystrophic muscle, and the genetic loss of uPA in mdx mice exacerbated muscle dystrophy and reduced muscular function. Bone marrow (BM) transplantation experiments revealed a critical function for BM-derived uPA in mdx muscle repair via three mechanisms: (1) by promoting the infiltration of BM-derived inflammatory cells; (2) by preventing the excessive deposition of fibrin; and (3) by promoting myoblast migration. Interestingly, genetic loss of the uPA receptor in mdx mice did not exacerbate muscular dystrophy in mdx mice, suggesting that uPA exerts its effects independently of its receptor. These findings underscore the importance of uPA in muscular dystrophy.
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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.