ArticleScientific reports2020
Cellular senescence-mediated exacerbation of Duchenne muscular dystrophy.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 74 citations in OpenAlex.
- Swallowing Dysfunction and Histopathological Changes in a Rat Model of Duchenne Muscular Dystrophy.Dysphagia · 2026Article
- A high-fat, high-sucrose diet exacerbates muscle and metabolic pathology and undermines glucocorticoid efficacy in dystrophin-deficient mice.The Journal of physiology · 2026Article
- Duchenne muscular dystrophy: from gene to gene-ius therapies.Skeletal muscle · 2026Review
- Senescence dynamics define therapeutic windows for Duchenne muscular dystrophy in DBA/2-mdx mice.Skeletal muscle · 2026Article
- Senescent-Like Myofibers Contribute to Anti-Regenerative Cytokine Signaling in Duchenne Muscular Dystrophy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Virus-induced endothelial senescence as a cause and driving factor for ME/CFS and long COVID: mediated by a dysfunctional immune system.Cell death & disease · 2026Review
- Targeting cellular senescence in dystrophinPharmacological research · 2025Article
- Cell therapy for Duchenne muscular dystrophy: promises, challenges, and controversies.Cellular and molecular life sciences : CMLS · 2025Review
- The rise of rat models for Duchenne muscular dystrophy and therapeutic evaluations.Skeletal muscle · 2025Review
- Ubiquitination-targeted therapies improve BMD iPSC myogenic cell engraftment and dystrophin expressionMolecular therapy. Methods & clinical development · 2025Article
- Continuous adipose-derived stem cell therapy from the neonatal stage effectively reduces Duchenne muscular dystrophy symptoms in rats.Stem cell research & therapy · 2025Article
- Bioactive lipid mediator class switching regulates myogenic cell progression and muscle regeneration.Nature communications · 2025Article
- Muscle stem cells in Duchenne muscular dystrophy exhibit molecular impairments and altered cell fate trajectories impacting regenerative capacity.Cell death & disease · 2025Article
- Forskolin treatment enhances muscle regeneration and shows therapeutic potential with limitations in Duchenne muscular dystrophy.Skeletal muscle · 2025Article
- New Horizons in Myotonic Dystrophy Type 1: Cellular Senescence as a Therapeutic Target.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- Stem/progenitor cell-based therapy for Duchenne muscular dystrophy.Frontiers in cell and developmental biology · 2025Review
- Emerging insights in senescence: pathways from preclinical models to therapeutic innovations.npj aging · 2024Review
- Review
- Dual FKRP/FST gene therapy normalizes ambulation, increases strength, decreases pathology, and amplifies gene expression in LGMDR9 mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Targeting Crosstalk of Signaling Pathways among Muscles-Bone-Adipose Tissue: A Promising Therapeutic Approach for Sarcopenia.Aging and disease · 2024Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Duchenne muscular dystrophy (DMD) is a progressive disease characterised by chronic muscle degeneration and inflammation. Our previously established DMD model rats (DMD rats) have a more severe disease phenotype than the broadly used mouse model. We aimed to investigate the role of senescence in DMD using DMD rats and patients. Senescence was induced in satellite cells and mesenchymal progenitor cells, owing to the increased expression of CDKN2A, p16- and p19-encoding gene. Genetic ablation of p16 in DMD rats dramatically restored body weight and muscle strength. Histological analysis showed a reduction of fibrotic and adipose tissues invading skeletal muscle, with increased muscle regeneration. Senolytic drug ABT263 prevented loss of body weight and muscle strength, and increased muscle regeneration in rats even at 8 months-the late stage of DMD. Moreover, senescence markers were highly expressed in the skeletal muscle of DMD patients. In situ hybridization of CDKN2A confirmed the expression of it in satellite cells and mesenchymal progenitor cells in patients with DMD. Collectively, these data provide new insights into the integral role of senescence in DMD progression.
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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.