ArticleHuman molecular genetics2015
The role of Notch signaling in muscle progenitor cell depletion and the rapid onset of histopathology in muscular dystrophy.
Article in Human molecular genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- PAX7, a Key for Myogenesis Modulation in Muscular Dystrophies through Multiple Signaling Pathways: A Systematic Review.International journal of molecular sciences · 2023Pooled it
- Targeting cellular senescence in dystrophinPharmacological research · 2025Article
- Article
- Extracellular matrix: Dystroglycan interactions-Roles for the dystrophin-associated glycoprotein complex in skeletal tissue dynamics.International journal of experimental pathology · 2025Review
- Article
- mtDNA release promotes cGAS-STING activation and accelerated aging of postmitotic muscle cells.Cell death & disease · 2024Article
- Precise large-fragment deletions in mammalian cells and mice generated by dCas9-controlled CRISPR/Cas3.Science advances · 2024Article
- Neurofibromin 1 controls metabolic balance and Notch-dependent quiescence of murine juvenile myogenic progenitors.Nature communications · 2024Article
- Satellite cell contribution to disease pathology in Duchenne muscular dystrophy.Frontiers in physiology · 2023Review
- Notch signaling leads to a slower progression of embryonic myogenic differentiation in Landrace than in Langtang pigs.Acta biochimica et biophysica Sinica · 2022Article
- Functional Identification of PorcineAnimals : an open access journal from MDPI · 2022Article
- Notch signaling pathway: architecture, disease, and therapeutics.Signal transduction and targeted therapy · 2022Review
- Implications of notch signaling in duchenne muscular dystrophy.Frontiers in physiology · 2022Review
- Therapeutic aspects of cell signaling and communication in Duchenne muscular dystrophy.Cellular and molecular life sciences : CMLS · 2021Review
- Diverse Roles of Cellular Senescence in Skeletal Muscle Inflammation, Regeneration, and Therapeutics.Frontiers in pharmacology · 2021Review
- Article
- Functional skeletal muscle constructs from transdifferentiated human fibroblasts.Scientific reports · 2020Article
- Echocardiographic signs of subclinical cardiac function impairment in Duchenne dystrophy gene carriers.Scientific reports · 2020Article
- The nSMase2/Smpd3 gene modulates the severity of muscular dystrophy and the emotional stress response in mdx mice.BMC medicine · 2020Article
- Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Although it has been speculated that stem cell depletion plays a role in the rapid progression of the muscle histopathology associated with Duchenne Muscular Dystrophy (DMD), the molecular and cellular mechanisms responsible for stem cell depletion remain poorly understood. The rapid depletion of muscle stem cells has not been observed in the dystrophin-deficient model of DMD (mdx mouse), which may explain the relatively mild dystrophic phenotype observed in this animal model. In contrast, we have observed a rapid occurrence of stem cell depletion in the dystrophin/utrophin double knockout (dKO) mouse model, which exhibits histopathological features that more closely recapitulate the phenotype observed in DMD patients compared with the mdx mouse. Notch signaling has been found to be a key regulator of stem cell self-renewal and myogenesis in normal skeletal muscle; however, little is known about the role that Notch plays in the development of the dystrophic histopathology associated with DMD. Our results revealed an over-activation of Notch in the skeletal muscles of dKO mice, which correlated with sustained inflammation, impaired muscle regeneration and the rapid depletion and senescence of the muscle progenitor cells (MPCs, i.e. Pax7+ cells). Consequently, the repression of Notch in the skeletal muscle of dKO mice delayed/reduced the depletion and senescence of MPCs, and restored the myogenesis capacity while reducing inflammation and fibrosis. We suggest that the down-regulation of Notch could represent a viable approach to reduce the dystrophic histopathologies associated with 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.