ArticleBMC musculoskeletal disorders2017
Treatment with soluble activin type IIB-receptor improves bone mass and strength in a mouse model of Duchenne muscular dystrophy.
Article in BMC musculoskeletal disorders, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- TGF-β/BMP signaling in skeletal biology: molecular mechanisms, regulatory networks, and therapeutic implications in development, regeneration, and disease.Bone research · 2026Review
- Research progress on sarcopenia in the musculoskeletal system.Bone research · 2025Review
- Roles of myokines in osteoporosis under physiological and diabetic conditions.Frontiers in endocrinology · 2025Review
- Poor bone health in Duchenne muscular dystrophy: a multifactorial problem beyond corticosteroids and loss of ambulation.Frontiers in endocrinology · 2024Review
- Peak Bone Mass Formation: Modern View of the Problem.Biomedicines · 2023Review
- Treatment with Soluble Activin Type IIB Receptor Ameliorates Ovariectomy-Induced Bone Loss and Fat Gain in Mice.Calcified tissue international · 2022Article
- Structures of activin ligand traps using natural sets of type I and type II TGFβ receptors.iScience · 2022Article
- Influencing Factors and Molecular Pathogenesis of Sarcopenia and Osteosarcopenia in Chronic Liver Disease.Life (Basel, Switzerland) · 2021Review
- Characterization of tolloid-mediated cleavage of the GDF8 procomplex.The Biochemical journal · 2021Article
- Bone Geometry Is Altered by Follistatin-Induced Muscle Growth in Young Adult Male Mice.JBMR plus · 2021Article
- An Overview of the Molecular Mechanisms Contributing to Musculoskeletal Disorders in Chronic Liver Disease: Osteoporosis, Sarcopenia, and Osteoporotic Sarcopenia.International journal of molecular sciences · 2021Review
- Deciphering Myostatin's Regulatory, Metabolic, and Developmental Influence in Skeletal Diseases.Frontiers in genetics · 2021Review
- Muscle NADMolecular metabolism · 2020Article
- Review
- Therapeutic and lifestyle approaches to obesity in older persons.Current opinion in clinical nutrition and metabolic care · 2019Review
- Targeting the Muscle-Bone Unit: Filling Two Needs with One Deed in the Treatment of Duchenne Muscular Dystrophy.Current osteoporosis reports · 2018Review
- Skeletal Response to Soluble Activin Receptor Type IIB in Mouse Models of Osteogenesis Imperfecta.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2018Article
- Anabolic Strategies to Augment Bone Fracture Healing.Current osteoporosis reports · 2018Review
- Effective regeneration of dystrophic muscle using autologous iPSC-derived progenitors with CRISPR-Cas9 mediated precise correction.Medical hypotheses · 2018Article
- ACVR2B/Fc counteracts chemotherapy-induced loss of muscle and bone mass.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
9 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundInhibition of activin/myostatin pathway has emerged as a novel approach to increase muscle mass and bone strength. Duchenne muscular dystrophy (DMD) is a neuromuscular disorder that leads to progressive muscle degeneration and also high incidence of fractures. The aim of our study was to test whether inhibition of activin receptor IIB ligands with or without exercise could improve bone strength in the mdx mouse model for DMD.
methodsThirty-two mdx mice were divided to running and non-running groups and to receive either PBS control or soluble activin type IIB-receptor (ActRIIB-Fc) once weekly for 7 weeks.
resultsTreatment of mdx mice with ActRIIB-Fc resulted in significantly increased body and muscle weights in both sedentary and exercising mice. Femoral μCT analysis showed increased bone volume and trabecular number (BV/TV +80%, Tb.N +70%, P < 0.05) in both ActRIIB-Fc treated groups. Running also resulted in increased bone volume and trabecular number in PBS-treated mice. However, there was no significant difference in trabecular bone structure or volumetric bone mineral density between the ActRIIB-Fc and ActRIIB-Fc-R indicating that running did not further improve bone structure in ActRIIB-Fc-treated mice. ActRIIB-Fc increased bone mass also in vertebrae (BV/TV +20%, Tb.N +30%, P < 0.05) but the effects were more modest. The number of osteoclasts was decreased in histological analysis and the expression of several osteoblast marker genes was increased in ActRIIB-Fc treated mice suggesting decreased bone resorption and increased bone formation in these mice. Increased bone mass in femurs translated into enhanced bone strength in biomechanical testing as the maximum force and stiffness were significantly elevated in ActRIIB-Fc-treated mice.
conclusionsOur results indicate that treatment of mdx mice with the soluble ActRIIB-Fc results in a robust increase in bone mass, without any additive effect by voluntary running. Thus ActRIIB-Fc could be an attractive option in the treatment of musculoskeletal disorders.
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