ArticleAmerican journal of respiratory cell and molecular biology2021
RANKL Mediates Muscle Atrophy and Dysfunction in a Cigarette Smoke-induced Model of Chronic Obstructive Pulmonary Disease.
Article in American journal of respiratory cell and molecular biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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32 citing papers in PubMed, 39 citations in OpenAlex.
- Age-dependent musculoskeletal changes during mechanical unloading with bisphosphonate treatment.Bone · 2026Article
- Mitochondrial and Epigenetic Drivers of Skeletal Muscle Dysfunction in Chronic Obstructive Pulmonary Disease.Antioxidants (Basel, Switzerland) · 2026Review
- RNA-binding protein hnRNPK: a multifunctional regulator of skeletal muscle biology and disease.Biochemical Society transactions · 2026Review
- Vascular and musculoskeletal interactions: structure, function, and therapeutic strategies for sarcopenia and osteoporosis.MedScience · 2026Review
- RANKL promotes airway inflammation via pro-inflammatory alveolar macrophage activation in COPD.Respiratory research · 2026Article
- Muscle-lung crosstalk in COPD: how exercise training modulates protein metabolism and inflammation in experimental COPD models.Frontiers in immunology · 2026Review
- RANKL-RANK signaling promotes cigarette smoke-induced emphysema with MMP-9 upregulation in alveolar macrophages.Frontiers in pharmacology · 2026Article
- Adipose-Muscle Crosstalk in COPD Cachexia: Early Adipose Atrophy Drives Subsequent Muscle Wasting.Journal of cachexia, sarcopenia and muscle · 2025Article
- Glucocorticoid-Mediated Skeletal Muscle Atrophy: Molecular Mechanisms and Potential Therapeutic Targets.International journal of molecular sciences · 2025Review
- ADAMTS4 Reduction Contributes to Extracellular Matrix Deposition and Impaired Myogenesis in the Skeletal Muscle of Cigarette Smoke-Exposed Mice.Biomedicines · 2025Article
- Cigarette Smoking Induces Skeletal Muscle Atrophy in Mice by Activated Macrophage-Mediated Pyroptosis.Journal of inflammation research · 2025Article
- Mechanism underlying the therapeutic effects of effective component compatibility of Bufei Yishen formula III combined with exercise rehabilitation on chronic obstructive pulmonary disease.Annals of medicine · 2024Article
- Extra-osseous Roles of the RANK-RANKL-OPG Axis with a Focus on Skeletal Muscle.Current osteoporosis reports · 2024Review
- The role of osteopontin and osteocyte-derived factors in secondary hyperparathyroidism-induced myopathy.JBMR plus · 2024Article
- TNFSF11/TNFRSF11A Axis Amplifies HDM-Induced Airway Remodeling by Strengthening TGFβ1/STAT3 Action.Allergy, asthma & immunology research · 2024Article
- The Impact of Non-bone Metastatic Cancer on Musculoskeletal Health.Current osteoporosis reports · 2024Review
- A non-invasive mouse model that recapitulates disuse-induced muscle atrophy in immobilized patients.Scientific reports · 2023Article
- Metabolic Health and Disease: A Role of Osteokines?Calcified tissue international · 2023Review
- Glycyl-l-histidyl-l-lysine-CuJournal of cachexia, sarcopenia and muscle · 2023Article
- An alternative mechanism for skeletal muscle dysfunction in long-term post-viral lung disease.American journal of physiology. Lung cellular and molecular physiology · 2023Article
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7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Skeletal muscle dysfunction is one of the important comorbidities of chronic obstructive pulmonary disease (COPD); however, the underlying mechanisms remain largely unknown. RANKL (receptor activator of nuclear factor κB ligand), a key mediator in osteoclast differentiation, was also found to play a role in skeletal muscle pathogenesis. Whether RANKL is involved in COPD-related skeletal muscle dysfunction is as-of-yet unknown. We examined the expression of RANKL/RANK in skeletal muscles from mice exposed to cigarette smoke (CS) for 24 weeks. Grip strength and exercise capacity as well as muscular morphology were evaluated in CS-exposed mice with or without anti-RANKL treatment. The expressions of protein synthesis- or muscle growth-related molecules (IGF-1, myogenin, and myostatin), muscle-specific ubiquitin E3 ligases (MuRF1 and atrogin-1), and the NF-κb inflammatory pathway were also evaluated in skeletal muscles. The effect of CS extract on RANKL/RANK expression and that of exogenous RANKL on the ubiquitin-proteasome pathway in C2C12 myotubes were investigated
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