ArticleProceedings of the National Academy of Sciences of the United States of America2012
Deletion of periostin reduces muscular dystrophy and fibrosis in mice by modulating the transforming growth factor-β pathway.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.
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Who cites it
93 citing papers in PubMed, 147 citations in OpenAlex.
- Conserved skeletal muscle transcriptomic responses to pacing strategies in Thoroughbred horses.Biology open · 2026Article
- CAR-T cells targeting fibroblast activation protein eliminate pathological fibroblasts and preserve cardiac function in a Duchenne Muscular Dystrophy murine model.Stem cell research & therapy · 2026Article
- Mining candidate genes for meat tenderness in Qinchuan cattle based on transcriptome analysis.BMC genomics · 2026Article
- Proteomics-based evaluation of AAV dystrophin gene therapy outcomes in mdx skeletal muscle.JCI insight · 2026Article
- Association of serum periostin with bone microarchitecture, muscle mass and function in Chinese postmenopausal women.Frontiers in endocrinology · 2026Article
- Epigenetic dysregulation in aged muscle stem cells drives mesenchymal progenitor expansion via IL-6 and Spp1 signaling.Nature aging · 2025Article
- Loss of cell-autonomously secreted laminin-α2 drives muscle stem cell dysfunction in LAMA2-related muscular dystrophy.Nature communications · 2025Article
- Extracellular matrix deposition precedes muscle-tendon integration during murine forelimb morphogenesis.Communications biology · 2025Article
- Periostin mediates collagen production, ECM remodeling and myofibroblast differentiation in breast prosthesis capsule formation.Scientific reports · 2025Article
- Obesity-driven musculotendinous remodeling impairs tissue resilience to mechanical damage.Cell and tissue research · 2025Article
- Klotho Is Cardioprotective in the mdx Mouse Model of Duchenne Muscular Dystrophy.The American journal of pathology · 2025Article
- Collagen type VI regulates TGF-β bioavailability in skeletal muscle in mice.The Journal of clinical investigation · 2025Article
- Distinct muscle regenerative capacity of human induced pluripotent stem cell-derived mesenchymal stromal cells in Ullrich congenital muscular dystrophy model mice.Stem cell research & therapy · 2024Article
- Functional cardiac consequences of β-adrenergic stress-induced injury in a model of Duchenne muscular dystrophy.Disease models & mechanisms · 2024Article
- Cell type mapping of inflammatory muscle diseases highlights selective myofiber vulnerability in inclusion body myositis.Nature aging · 2024Article
- Targeted Antisense Oligonucleotide-Mediated Skipping of MurineInternational journal of molecular sciences · 2024Article
- The extracellular matrix differentially directs myoblast motility and differentiation in distinct forms of muscular dystrophy: Dystrophic matrices alter myoblast motility.Matrix biology : journal of the International Society for Matrix Biology · 2024Article
- Functional cardiac consequences of β-adrenergic stress-induced injury in thebioRxiv : the preprint server for biology · 2024Article
- Periostin-TGF-β feedforward loop contributes to tumour-stroma crosstalk in liver metastatic outgrowth of colorectal cancer.British journal of cancer · 2024Article
- Expression of the Pro-Fibrotic Marker Periostin in a Mouse Model of Duchenne Muscular Dystrophy.Biomedicines · 2024Article
33 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
Abstract
The muscular dystrophies are broadly classified as muscle wasting diseases with myofiber dropout due to cellular necrosis, inflammation, alterations in extracellular matrix composition, and fatty cell replacement. These events transpire and progress despite ongoing myofiber regeneration from endogenous satellite cells. The degeneration/regeneration response to muscle injury/disease is modulated by the proinflammatory cytokine transforming growth factor-β (TGF-β), which can also profoundly influence extracellular matrix composition through increased secretion of profibrotic proteins, such as the matricellular protein periostin. Here we show that up-regulation and secretion of periostin is pathological and enhances disease in the δ-sarcoglycan null (Sgcd(-/-)) mouse model of muscular dystrophy (MD). Indeed, MD mice lacking the Postn gene showed dramatic improvement in skeletal muscle structure and function. Mechanistically, Postn gene deletion altered TGF-β signaling so that it now enhanced tissue regeneration with reduced levels of fibrosis. Systemic antagonism of TGF-β with a neutralizing monoclonal antibody mitigated the beneficial effects of Postn deletion in vivo. These data suggest that periostin functions as a disease determinant in MD by promoting/allowing the pathological effects of TGF-β, suggesting that inhibition of periostin could represent a unique treatment approach.
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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.