ArticleThe Journal of biological chemistry2016
Cathepsin S Contributes to the Pathogenesis of Muscular Dystrophy in Mice.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- Neuromuscular Electrical Stimulation to Combat Muscle Atrophy During Spaceflight: A Narrative Review of Mechanisms and Potential Applications.Life (Basel, Switzerland) · 2026Review
- Relationship between cathepsin K and extracellular matrix dynamics: a comprehensive review.Frontiers in oncology · 2026Review
- Lysosomal damage is a therapeutic target in Duchenne muscular dystrophy.Science advances · 2025Article
- Cathepsin S activity controls chronic stress-induced muscle atrophy and dysfunction in mice.Cellular and molecular life sciences : CMLS · 2023Article
- [Research advances in pharmacotherapy for rare diseases in children].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2023Review
- The myokine Fibcd1 is an endogenous determinant of myofiber size and mitigates cancer-induced myofiber atrophy.Nature communications · 2022Article
- Identification of immune-related features involved in Duchenne muscular dystrophy: A bidirectional transcriptome and proteome-driven analysis.Frontiers in immunology · 2022Article
- Physiological effects of inactivation and the roles of Elovl3/ELOVL3 in maintaining ocular homeostasis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Transcriptome and DNA Methylation Profiles of Mouse Fetus and Placenta Generated by Round Spermatid Injection.Frontiers in cell and developmental biology · 2021Article
- Cathepsin S: investigating an old player in lung disease pathogenesis, comorbidities, and potential therapeutics.Respiratory research · 2020Review
- Plasma proteomic signature of the risk of developing mobility disability: A 9-year follow-up.Aging cell · 2020Article
- Genome-Wide RNAi Screen Identifies Regulators of Cardiomyocyte Necrosis.ACS pharmacology & translational science · 2019Article
- miR-146a deficiency does not aggravate muscular dystrophy in mdx mice.Skeletal muscle · 2019Article
- Thrombospondin-3 augments injury-induced cardiomyopathy by intracellular integrin inhibition and sarcolemmal instability.Nature communications · 2019Article
- β1-Integrin Deletion From the Lens Activates Cellular Stress Responses Leading to Apoptosis and Fibrosis.Investigative ophthalmology & visual science · 2017Article
- Investigating the Life Expectancy and Proteolytic Degradation of Engineered Skeletal Muscle Biological Machines.Scientific reports · 2017Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Duchenne muscular dystrophy (DMD) is an X-linked recessive disease caused by mutations in the gene encoding dystrophin. Loss of dystrophin protein compromises the stability of the sarcolemma membrane surrounding each muscle cell fiber, leading to membrane ruptures and leakiness that induces myofiber necrosis, a subsequent inflammatory response, and progressive tissue fibrosis with loss of functional capacity. Cathepsin S (Ctss) is a cysteine protease that is actively secreted in areas of tissue injury and ongoing inflammation, where it participates in extracellular matrix remodeling and healing. Here we show significant induction of Ctss expression and proteolytic activity following acute muscle injury or in muscle from mdx mice, a model of DMD. To examine the functional ramifications associated with greater Ctss expression, the Ctss gene was deleted in the mdx genetic background, resulting in protection from muscular dystrophy pathogenesis that included reduced myofiber turnover and histopathology, reduced fibrosis, and improved running capacity. Mechanistically, deletion of the Ctss gene in the mdx background significantly increased myofiber sarcolemmal membrane stability with greater expression and membrane localization of utrophin, integrins, and β-dystroglycan, which anchor the membrane to the basal lamina and underlying cytoskeletal proteins. Consistent with these results, skeletal muscle-specific transgenic mice overexpressing Ctss showed increased myofiber necrosis, muscle histopathology, and a functional deficit reminiscent of muscular dystrophy. Hence, Ctss induction during muscular dystrophy is a pathologic event that partially underlies disease pathogenesis, and its inhibition might serve as a new therapeutic strategy in 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.