ArticleJournal of cachexia, sarcopenia and muscle2022
Cathelicidin-related antimicrobial peptide mediates skeletal muscle degeneration caused by injury and Duchenne muscular dystrophy in mice.
Article in Journal of cachexia, sarcopenia and muscle, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Aging induces sarcopenia by disrupting the crosstalk between the skeletal muscle microenvironment and myofibers.Journal of advanced research · 2026Review
- Complete Loss of Cramp Promotes Experimental Osteoarthritis with Enhanced Chondrocyte Apoptosis in Mice.International journal of molecular sciences · 2025Article
- Long-Term Dietary Consumption of Grapes Alters Phenotypic Expression in Skeletal Muscle of Aged Male and Female Mice.Foods (Basel, Switzerland) · 2025Article
- Temporal dynamics of the interstitial fluid proteome in human skeletal muscle following exhaustive exercise.Science advances · 2025Article
- Scientific and Technological Prospecting on Polymeric Particles Containing Extracellular Matrix Peptides for the Treatment of Duchenne Muscular Dystrophy.Recent advances in drug delivery and formulation · 2025Review
- Inhibition of MAT2A Impairs Skeletal Muscle Repair Function.Biomolecules · 2024Article
- A Novel MAO-B/SSAO Inhibitor Improves Multiple Aspects of Dystrophic Phenotype inAntioxidants (Basel, Switzerland) · 2024Article
- LL-37 Might Promote Local Invasion of Melanoma by Activating Melanoma Cells and Tumor-Associated Macrophages.Cancers · 2023Article
- Cathelicidin-related antimicrobial peptide mediates skeletal muscle degeneration caused by injury and Duchenne muscular dystrophy in mice.Journal of cachexia, sarcopenia and muscle · 2022Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCathelicidin, an antimicrobial peptide, plays a key role in regulating bacterial killing and innate immunity; however, its role in skeletal muscle function is unknown. We investigated the potential role of cathelicidin in skeletal muscle pathology resulting from acute injury and Duchenne muscular dystrophy (DMD) in mice.
methodsExpression changes and muscular localization of mouse cathelicidin-related antimicrobial peptide (Cramp) were examined in the skeletal muscle of normal mice treated with chemicals (cardiotoxin and BaCl
resultsIn response to acute muscle injury, Cramp was activated in muscle-infiltrating neutrophils and internalized into myofibres. Cramp treatments of mouse skeletal muscles or C2C12 myotubes resulted in muscle degeneration and myotube damage, respectively. Genetic ablation of Cramp reduced neutrophil infiltration and ameliorated muscle pathology, such as fibre size (P < 0.001; n = 6) and fibrofatty infiltration (P < 0.05). Genetic reduction of Cramp in mdx/Utrn
conclusionsThese findings identify Cramp as an immune cell-derived regulator of skeletal muscle degeneration and provide a potential therapeutic target for DMD.
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