ArticleScientific reports2022
Matrix stiffness and architecture drive fibro-adipogenic progenitors' activation into myofibroblasts.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 0 citations in OpenAlex.
- Review
- Phase-transition failure in aged skeletal muscle regeneration.Biogerontology · 2026Review
- Treating age-related loss of muscle mass and function: Where should we be focusing?The Journal of physiology · 2026Review
- Hydrogels for Skeletal Muscle Regeneration: Design, Fabrication, and Future Applications.ACS polymers Au · 2026Review
- Phenotypic divergence in rotator cuff tear and volumetric muscle loss mouse models following fibroadipogenic progenitor depletion.Bone & joint research · 2026Article
- Collagen VI is a fibrosis-associated signal disrupting muscle regeneration across distinct human myopathies.EMBO reports · 2026Article
- Network medicine and single-cell mapping identify a collagen-rich, fibrosis-associated hub module in Duchenne muscular dystrophy.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Single cell analysis of muscle contracture in cerebral palsy reveals profibrotic and antimyogenic stem cell populations with altered cell-cell interactions.American journal of physiology. Cell physiology · 2026Article
- Article
- An animal component-free bioprocess for synthesizing 3D human matrix scaffolds using mesenchymal stromal cells.Frontiers in cell and developmental biology · 2026Article
- Matrix Stiffness Promotes DRP1-Mediated Myofibroblast Senescence to Drive Silica-Induced Pulmonary Fibrosis.Aging cell · 2025Article
- Fork in the road: therapeutic and pathological actions for fibro-adipogenic progenitors following musculoskeletal injury.The Journal of physiology · 2025Review
- Epigenetic dysregulation in aged muscle stem cells drives mesenchymal progenitor expansion via IL-6 and Spp1 signaling.Nature aging · 2025Article
- The role of muscle fascia in heterotopic ossification and maintenance of skeletal muscle integrity in fibrodysplasia ossificans progressiva.bioRxiv : the preprint server for biology · 2025Article
- Article
- From fibro/adipogenic progenitors to adipocytes: Understanding adipogenesis in muscle degeneration for disease modulation.The Journal of physiology · 2025Review
- Macrophage Polarization in Heterotopic Ossification: Inflammation, Osteogenesis, and Emerging Therapeutic Targets.International journal of molecular sciences · 2025Review
- Quercetin, Kaempferol and Capsaicin Counteract the TGF-β1-Induced Upregulation of αSMA and Collagen in Myoblasts.International journal of molecular sciences · 2025Article
- The impact of extracellular matrix proteins on bovine fibro-adipogenic progenitor cell adhesion, proliferation, and differentiation in vitro.Physiological reports · 2025Article
- Viscoelastic HyA Hydrogel Promotes Recovery of Muscle Quality and Vascularization in a Murine Model of Delayed Rotator Cuff Repair.Advanced healthcare materials · 2025Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Fibro-adipogenic progenitors (FAPs) are essential in supporting regeneration in skeletal muscle, but in muscle pathologies FAPs the are main source of excess extracellular matrix (ECM) resulting in fibrosis. Fibrotic ECM has altered mechanical and architectural properties, but the feedback onto FAPs of stiffness or ECM properties is largely unknown. In this study, FAPs' sensitivity to their ECM substrate was assessed using collagen coated polyacrylamide to control substrate stiffness and collagen hydrogels to engineer concentration, crosslinking, fibril size, and alignment. FAPs on substrates of fibrotic stiffnesses had increased myofibroblast activation, depicted by αSMA expression, compared to substrates mimicking healthy muscle, which correlated strongly YAP nuclear localization. Surprisingly, fibrosis associated collagen crosslinking and larger fibril size inhibited myofibroblast activation, which was independent of YAP localization. Additionally, collagen crosslinking and larger fibril diameters were associated with decreased remodeling of the collagenous substrate as measured by second harmonic generation imaging. Inhibition of YAP activity through verteporfin reduced myofibroblast activation on stiff substrates but not substrates with altered architecture. This study is the first to demonstrate that fibrotic muscle stiffness can elicit FAP activation to myofibroblasts through YAP signaling. However, fibrotic collagen architecture actually inhibits myofibroblast activation through a YAP independent mechanism. These data expand knowledge of FAPs sensitivity to ECM and illuminate targets to block FAP's from driving progression of muscle fibrosis.
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