ArticlePloS one2016
Activin Receptor Type IIB Inhibition Improves Muscle Phenotype and Function in a Mouse Model of Spinal Muscular Atrophy.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 3 of them syntheses that pooled it.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
33 citing papers in PubMed, 3 syntheses or guidelines pooled it, 35 citations in OpenAlex.
- Myostatin Modulation in Spinal Muscular Atrophy: A Systematic Review of Preclinical and Clinical Evidence.International journal of molecular sciences · 2025Pooled it
- Drug treatment for spinal muscular atrophy types II and III.The Cochrane database of systematic reviews · 2020Pooled it
- Drug treatment for spinal muscular atrophy type I.The Cochrane database of systematic reviews · 2019Pooled it
- Safety and Efficacy of Apitegromab in Patients With Spinal Muscular Atrophy Types 2 and 3: The Phase 2 TOPAZ Study.Neurology · 2024Trial
- Genetic and Pharmacologic Inhibition of Myostatin Restores Muscle Mass in a Dynamin 2-Related Centronuclear Myopathy Mouse Model.Journal of cachexia, sarcopenia and muscle · 2026Article
- Sarcopenia and Skeletal Muscle Dysfunction in Liver Cirrhosis: Clinical Perspectives of Myostatin Inhibition.Biomedicines · 2026Review
- UBA1 knockdown dysregulates UBA1-sensitive proteins and impairs muscle function in models of spinal muscular atrophy X-linked 2.Disease models & mechanisms · 2026Article
- ACE-031, a soluble activin type IIB receptor, increases muscle mass and strength in the common marmoset (Callithrix jacchus).PloS one · 2026Article
- ACE-031, a Soluble Activin Type IIB Receptor, Increases Muscle Mass and Strength in the Common Marmoset (Callithrix jacchus).bioRxiv : the preprint server for biology · 2025Article
- The effect of coadministration of D156844 and AR42 (REC-2282) on the survival and motor phenotype of mice with spinal muscular atrophy.Scientific reports · 2025Article
- Klf9 Loss of Function Protects Against Glucocorticoids Induced Skeletal Muscle Wasting.Journal of cachexia, sarcopenia and muscle · 2025Article
- Review
- The Role of Myokines in Liver Diseases.International journal of molecular sciences · 2025Review
- Impact of Disease Severity and Disease-Modifying Therapies on Myostatin Levels in SMA Patients.International journal of molecular sciences · 2024Article
- Improved therapeutic approach for spinal muscular atrophy via ubiquitination-resistant survival motor neuron variant.Journal of cachexia, sarcopenia and muscle · 2024Article
- Serum myostatin as a candidate disease severity and progression biomarker of spinal muscular atrophy.Brain communications · 2024Article
- Muscle: an independent contributor to the neuromuscular spinal muscular atrophy disease phenotype.JCI insight · 2023Review
- Platelet-derived chemokines promote skeletal muscle regeneration by guiding neutrophil recruitment to injured muscles.Nature communications · 2023Article
- Progressive development of melanoma-induced cachexia differentially impacts organ systems in mice.Cell reports · 2023Article
- Protective Effect of Delta-Like 1 Homolog Against Muscular Atrophy in a Mouse Model.Endocrinology and metabolism (Seoul, Korea) · 2022Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Spinal muscular atrophy (SMA) is a devastating neurodegenerative disorder that causes progressive muscle atrophy and weakness. Using adeno-associated virus-mediated gene transfer, we evaluated the potential to improve skeletal muscle weakness via systemic, postnatal inhibition of either myostatin or all signaling via the activin receptor type IIB (ActRIIB). After demonstrating elevated p-SMAD3 content and differential content of ActRIIB ligands, 4-week-old male C/C SMA model mice were treated intraperitoneally with 1x1012 genome copies of pseudotype 2/8 virus encoding a soluble form of the ActRIIB extracellular domain (sActRIIB) or protease-resistant myostatin propeptide (dnMstn) driven by a liver specific promoter. At 12 weeks of age, muscle mass and function were improved in treated C/C mice by both treatments, compared to controls. The fast fiber type muscles had a greater response to treatment than did slow muscles, and the greatest therapeutic effects were found with sActRIIB treatment. Myostatin/activin inhibition, however, did not rescue C/C mice from the reduction in motor unit numbers of the tibialis anterior muscle. Collectively, this study indicates that myostatin/activin inhibition represents a potential therapeutic strategy to increase muscle mass and strength, but not neuromuscular junction defects, in less severe forms of SMA.
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Registered trials
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