ArticleScientific reports2016
CL316,243, a β3-adrenergic receptor agonist, induces muscle hypertrophy and increased strength.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- Exosome trafficking is a key regulator of adipocyte thermogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Age-related changes in adrenergic regulation of contractility and redox status of glycolytic and oxidative skeletal muscles.GeroScience · 2026Article
- Exposure to predator threat engages sympathetic nervous system outflow to skeletal muscle.Autonomic neuroscience : basic & clinical · 2025Article
- Cold Exposure Drives Weight Gain and Adiposity following Chronic Suppression of Brown Adipose Tissue.International journal of molecular sciences · 2022Article
- The β3 Adrenergic Receptor Agonist CL316243 Ameliorates the Metabolic Abnormalities of High-Fat Diet-Fed Rats by Activating AMPK/PGC-1α Signaling in Skeletal Muscle.Diabetes, metabolic syndrome and obesity : targets and therapy · 2021Article
- Single Cell ADNP Predictive of Human Muscle Disorders: Mouse Knockdown Results in Muscle Wasting.Cells · 2020Article
- DMD Pluripotent Stem Cell Derived Cardiac Cells RecapitulateFrontiers in bioengineering and biotechnology · 2020Article
- Everything You Always Wanted to Know about βCells · 2019Review
- Respiratory dysfunction following initiation of mirabegron: A case report.Respiratory medicine case reports · 2019Article
- Evaluation of Muscle Performance in Mice by Treadmill Exhaustion Test and Whole-limb Grip Strength Assay.Bio-protocol · 2017Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Studies in vitro have demonstrated that β3-adrenergic receptors (β3-ARs) regulate protein metabolism in skeletal muscle by promoting protein synthesis and inhibiting protein degradation. In this study, we evaluated whether activation of β3-ARs by the selective agonist CL316,243 modifies the functional and structural properties of skeletal muscles of healthy mice. Daily injections of CL316,243 for 15 days resulted in a significant improvement in muscle force production, assessed by grip strength and weight tests, and an increased myofiber cross-sectional area, indicative of muscle hypertrophy. In addition, atomic force microscopy revealed a significant effect of CL316,243 on the transversal stiffness of isolated muscle fibers. Interestingly, the expression level of mammalian target of rapamycin (mTOR) downstream targets and neuronal nitric oxide synthase (NOS) was also found to be enhanced in tibialis anterior and soleus muscles of CL316,243 treated mice, in accordance with previous data linking β3-ARs to mTOR and NOS signaling pathways. In conclusion, our data suggest that CL316,243 systemic administration might be a novel therapeutic strategy worthy of further investigations in conditions of muscle wasting and weakness associated with aging and muscular diseases.
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