ArticleBMC biology2018
Downregulation of the NLRP3 inflammasome by adiponectin rescues Duchenne muscular dystrophy.
Article in BMC biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 73 citations in OpenAlex.
- Identification of myokines associated with the pathological stress response in theJournal of neuromuscular diseases · 2026Article
- Emerging roles of microRNAs and other non-coding transcriptome in muscular dystrophies.Inflammation and regeneration · 2026Review
- Muscle transcriptome profiling reveals novel molecular pathways and biomarkers in laminin-α2 deficient patients.Acta neuropathologica communications · 2026Article
- Acid ceramidase as a novel target for adiponectin receptor agonist to abrogate podocyte NLRP3 inflammasome activation and glomerular inflammation during obesity.The Journal of pharmacology and experimental therapeutics · 2025Article
- Deubiquitinases in muscle physiology and disorders.Biochemical Society transactions · 2024Review
- Recent Advances in Pre-Clinical Development of Adiponectin Receptor Agonist Therapies for Duchenne Muscular Dystrophy.Biomedicines · 2024Review
- NLRP3 Contributes to Sarcopenia Associated to Dependency Recapitulating Inflammatory-Associated Muscle Degeneration.International journal of molecular sciences · 2024Article
- The genetic advantage of healthy centenarians: unraveling the central role of NLRP3 in exceptional healthspan.Frontiers in aging · 2024Review
- The Relationship Between the Serum NLRP3 and Adiponectin Levels and Coronary Lesions in Patients with Unstable Angina with Type 2 Diabetes.Clinical interventions in aging · 2024Article
- Comprehensive cardiac magnetic resonance T1, T2, and extracellular volume mapping to define Duchenne cardiomyopathy.Journal of cardiovascular magnetic resonance : official journal of the Society for Cardiovascular Magnetic Resonance · 2023Article
- Inflammasome in Skeletal Muscle: NLRP3 Is an Inflammatory Cell Stress Component in Inclusion Body Myositis.International journal of molecular sciences · 2023Article
- The Contribution of Muscle Innate Immunity to Uremic Cachexia.Nutrients · 2023Review
- The Role of P2X7 Purinoceptors in the Pathogenesis and Treatment of Muscular Dystrophies.International journal of molecular sciences · 2023Review
- Inflammasome Activity in the Skeletal Muscle and Heart of Rodent Models for Duchenne Muscular Dystrophy.International journal of molecular sciences · 2023Article
- Targeting gut dysbiosis against inflammation and impaired autophagy in Duchenne muscular dystrophy.EMBO molecular medicine · 2023Article
- TRIM72 Alleviates Muscle Inflammation in mdx Mice via Promoting Mitophagy-Mediated NLRP3 Inflammasome Inactivation.Oxidative medicine and cellular longevity · 2023Article
- Inflammasome pathway in kidney transplantation.Frontiers in medicine · 2023Review
- Mechanisms of Myofibre Death in Muscular Dystrophies: The Emergence of the Regulated Forms of Necrosis in Myology.International journal of molecular sciences · 2022Review
- COVID-19 Mimics Pulmonary Dysfunction in Muscular Dystrophy as a Post-Acute Syndrome in Patients.International journal of molecular sciences · 2022Review
- Histological Methods to Assess Skeletal Muscle Degeneration and Regeneration in Duchenne Muscular Dystrophy.International journal of molecular sciences · 2022Review
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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
backgroundThe hormone adiponectin (ApN) exerts powerful anti-inflammatory effects on skeletal muscle and can reverse devastating myopathies, like Duchenne muscular dystrophy (DMD), where inflammation exacerbates disease progression. The NLRP3 inflammasome plays a key role in the inflammation process, and its aberrant activation leads to several inflammatory or immune diseases. Here we investigated the expression of the NLRP inflammasome in skeletal muscle and its contribution to DMD.
resultsWe find that NLRP3 is expressed in skeletal muscle and show that ApN downregulates NLRP3 via its anti-inflammatory mediator, miR-711. This repression occurs both in vitro in C2C12 myotubes and in vivo after either local (via muscle electrotransfer) or systemic (by using transgenic mice) ApN supplementation. To explore the role of the NLRP3 inflammasome in a murine model of DMD, we crossed mdx mice with Nlrp3-knockout mice. In mdx mice, all components of the inflammasome were upregulated in muscle, and the complex was overactivated. By contrast, in mdx mice lacking Nlrp3, there was a reduction in caspase-1 activation, inflammation and oxidative stress in dystrophic muscle, and these mice showed higher global muscle force/endurance than regular mdx mice as well as decreased muscle damage. To investigate the relevance of NLPR3 regulation in a human disease context, we characterized NLRP3 expression in primary cultures of myotubes from DMD subjects and found a threefold increase compared to control subjects. This overexpression was attenuated by ApN or miR-711 mimic treatments.
conclusionsThe NLRP3 inflammasome plays a key pathogenic role in DMD and muscle inflammation, thereby opening new therapeutic perspectives for these and other related disorders.
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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.