Osteoprotegerin Protects against Muscular Dystrophy
Open accessAbstract
Receptor-activator of NF-κB, its ligand RANKL, and the soluble decoy receptor osteoprotegerin are the key regulators of osteoclast differentiation and bone remodeling. Although there is a strong association between osteoporosis and skeletal muscle atrophy/dysfunction, the functional relevance of a particular biological pathway that synchronously regulates bone and skeletal muscle physiopathology still is elusive. Here, we show that muscle cells can produce and secrete osteoprotegerin and pharmacologic treatment of dystrophic mdx mice with recombinant osteoprotegerin muscles. (Recombinant osteoprotegerin-Fc mitigates the loss of muscle force in a dose-dependent manner and preserves muscle integrity, particularly in fast-twitch extensor digitorum longus.) Our data identify osteoprotegerin as a novel protector of muscle integrity, and it potentially represents a new therapeutic avenue for both muscular diseases and osteoporosis.
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OPG has been shown to be capable of increasing muscle force when given to mdx mice, a model for muscular dystrophy.
“In addition to the role that OPG plays in modulating RANK signaling in osteoclasts, OPG has been shown to be capable of increasing muscle force when given to mdx mice (39, 40), which is a model for muscular dystrophy, raising the possibility that OPG may play a role in muscle hypertrophy induced by loss of MSTN/activin A signaling.”
From Targeting myostatin/activin A protects against skeletal muscle and bone loss during spaceflight (2020) · cites this paper as [39]
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References 52 · Cited by 61
- Authors
- Dufresne, S. S., Dumont, N. A., Bouchard, P., Lavergne, É., Penninger, J. M., & Frenette, J.
- Affiliations
- Centre hospitalier de l'Université Laval (CA)
- Institute of Molecular Biotechnology (AT)
- Corresponding author
- Frenette, Jérôme
- Venue
- The American Journal of Pathology
- Publisher
- Elsevier BV
- Published
- 2015-04
- Volume
- 185
- Issue
- 4
- Pages
- 920-926
- ISSN
- 0002-9440 (ISSN-L)
- OpenAlex
- W2118842702
- Cited by
- 61
- References
- 52
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 4 · 2023: 8 · 2022: 4 · 2021: 10 · 2020: 7 · 2019: 5 · 2018: 7 · 2017: 3 · 2016: 6 · 2015: 1
- FWCI
- 2.46
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- American Journal Of Pathology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Canadian Institutes of Health Research (JNM-123675)
- Natural Sciences and Engineering Research Council of Canada (NSERC-227114)
- Muscular Dystrophy Canada
- Austrian Academy of Sciences
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
- Health Sciences › Medicine › Genetics › Neurogenetic and Muscular Disorders Research
- Keywords
- osteoprotegerin, muscular dystrophy, mdx mice, RANKL, skeletal muscle atrophy, muscle force, extensor digitorum longus, fast-twitch muscle, osteoporosis, muscle-bone crosstalk, muscle integrity
- MeSH terms
- Animals, Cell Line, Immunoglobulin Fc Fragments, Inflammation, Leukocytes, Lipopolysaccharides, Male, Mice, Inbred C57BL, Muscles, Muscular Dystrophy, Animal, Muscle Fibers, Skeletal, Osteoprotegerin, In Vitro Techniques
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