ArticleCellular and molecular life sciences : CMLS2017
Skeletal muscle secretome in Duchenne muscular dystrophy: a pivotal anti-inflammatory role of adiponectin.
Article in Cellular and molecular life sciences : CMLS, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- Pooled it
- Identification of myokines associated with the pathological stress response in theJournal of neuromuscular diseases · 2026Article
- CRISPR-Cas9-mediated upregulation of utrophin ameliorates Duchenne muscular dystrophy.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Recent Advances in Pre-Clinical Development of Adiponectin Receptor Agonist Therapies for Duchenne Muscular Dystrophy.Biomedicines · 2024Review
- Administration of adiponectin receptor agonist AdipoRon relieves cancer cachexia by mitigating inflammation in tumour-bearing mice.Journal of cachexia, sarcopenia and muscle · 2024Article
- The Adiponectin Receptor Agonist, ALY688: A Promising Therapeutic for Fibrosis in the Dystrophic Muscle.Cells · 2023Article
- Association between blood eosinophil count and Duchenne muscular dystrophy severity and prognosis: a retrospective cohort study.Italian journal of pediatrics · 2023Article
- Histone Deacetylases as Modulators of the Crosstalk Between Skeletal Muscle and Other Organs.Frontiers in physiology · 2022Review
- Review
- The Immune System in Duchenne Muscular Dystrophy Pathogenesis.Biomedicines · 2021Review
- Utrophin modulator drugs as potential therapies for Duchenne and Becker muscular dystrophies.Neuropathology and applied neurobiology · 2021Article
- Excess Glucose Impedes the Proliferation of Skeletal Muscle Satellite Cells Under Adherent Culture Conditions.Frontiers in cell and developmental biology · 2021Article
- Adipocytokines: Are they the Theory of Everything?Cytokine · 2020Review
- Adiponectin and Its Mimics on Skeletal Muscle: Insulin Sensitizers, Fat Burners, Exercise Mimickers, Muscling Pills … or Everything Together?International journal of molecular sciences · 2020Review
- AdipoRon, a new therapeutic prospect for Duchenne muscular dystrophy.Journal of cachexia, sarcopenia and muscle · 2020Article
- Adiponectin-Consideration for its Role in Skeletal Muscle Health.International journal of molecular sciences · 2019Review
- Adiponectin in Myopathies.International journal of molecular sciences · 2019Review
- Links Between Adiponectin and Dementia: From Risk Factors to Pathophysiology.Frontiers in aging neuroscience · 2019Article
- Skeletal Muscle Metabolism in Duchenne and Becker Muscular Dystrophy-Implications for Therapies.Nutrients · 2018Review
- Downregulation of the NLRP3 inflammasome by adiponectin rescues Duchenne muscular dystrophy.BMC biology · 2018Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPersistent inflammation exacerbates the progression of Duchenne muscular dystrophy (DMD). The hormone, adiponectin (ApN), which is decreased in the metabolic syndrome, exhibits anti-inflammatory properties on skeletal muscle and alleviates the dystrophic phenotype of mdx mice. Here, we investigate whether ApN retains its anti-inflammatory action in myotubes obtained from DMD patients. We unravel the underlying mechanisms by studying the secretome and the early events of ApN.
methodsPrimary cultures of myotubes from DMD and control patients were treated or not by ApN after an inflammatory challenge. Myokines secreted in medium were identified by cytokine antibody-arrays and ELISAs. The early events of ApN signaling were assessed by abrogating selected genes.
resultsApN retained its anti-inflammatory properties in both dystrophic and control myotubes. Profiling of secretory products revealed that ApN downregulated the secretion of two pro-inflammatory factors (TNFα and IL-17A), one soluble receptor (sTNFRII), and one chemokine (CCL28) in DMD myotubes, while upregulating IL-6 that exerts some anti-inflammatory effects. These changes were explained by pretranslational mechanisms. Earlier events of the ApN cascade involved AdipoR1, the main receptor for muscle, and the AMPK-SIRT1-PGC-1α axis leading, besides alteration of the myokine profile, to the upregulation of utrophin A (a dystrophin analog).
conclusionApN retains its beneficial properties in dystrophic muscles by activating the AdipoR1-AMPK-SIRT1-PGC-1α pathway, thereby inducing a shift in the secretion of downstream myokines toward a less inflammatory profile while upregulating utrophin. ApN, the early events of the cascade and downstream myokines may be therapeutic targets for the management of DMD.
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Registered trials
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