ArticleCell transplantation2012
Administration of a soluble activin type IIB receptor promotes the transplantation of human myoblasts in dystrophic mice.
Article in Cell transplantation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Inhibition ofFrontiers in cell and developmental biology · 2021Article
- Skeletal muscle cell transplantation: models and methods.Journal of muscle research and cell motility · 2020Article
- Stem cell therapy for muscular dystrophies.The Journal of clinical investigation · 2020Review
- Muscle xenografts reproduce key molecular features of facioscapulohumeral muscular dystrophy.Experimental neurology · 2019Article
- Centronuclear myopathies under attack: A plethora of therapeutic targets.Journal of neuromuscular diseases · 2018Review
- Molecular mechanisms and therapeutic interventions in sarcopenia.Osteoporosis and sarcopenia · 2017Review
- Functional validation and expression analysis of myotubes converted from skin fibroblasts using a simple direct reprogramming strategy.eNeurologicalSci · 2017Article
- Neuromuscular electrical stimulation promotes development in mice of mature human muscle from immortalized human myoblasts.Skeletal muscle · 2016Article
- Therapeutic advances in muscular dystrophy.Annals of neurology · 2013Review
- Article
- Optimization of Xenografting Methods for Generating Human Skeletal Muscle in Mice.Cell transplantationArticle
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Duchenne muscular dystrophy (DMD) is a recessive disease caused by a dystrophin gene mutation. Myoblast transplantation permits the introduction of the dystrophin gene into dystrophic muscle fibers. However, this strategy has so far produced limited results. Modulation of transforming growth factor-β (TGF-β) superfamily signaling promotes skeletal muscle differentiation and growth and myogenic regeneration. We investigated the possibility that the combination of TGF-β superfamily signaling inhibition with myoblast transplantation might be an effective therapeutic approach in dystrophin-deficient patients. In vitro, blocking myostatin and other ligands with a soluble form of the extracellular domain of the activin IIB receptor (ActRIIB/Fc) upregulated the expression of myogenic differentiation factors and increased human myoblast fusion. In vivo, systemic inhibition of activin IIB receptor signaling by delivery of ActRIIB/Fc increased the success of the myoblast transplantation. This effect was further increased by forcing the mice to swim weekly to induce cycles of muscle degeneration and regeneration. Treatment of dystrophic mice with ActRIIB/Fc led to increased body weight, increased skeletal muscle mass, and improved myoblast transplantation. Thus, ActRIIB/Fc represents an effective therapeutic strategy for muscular dystrophies, and its effects are enhanced when combined with muscle exercise.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.