ArticleThe Journal of pathology2015
Sustained β-catenin activity in dermal fibroblasts promotes fibrosis by up-regulating expression of extracellular matrix protein-coding genes.
Article in The Journal of pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
What it found
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Who cites it
68 citing papers in PubMed, 112 citations in OpenAlex.
- A Scoping Review of Emerging Treatments in the Pipeline for Idiopathic Pulmonary Fibrosis: Future Perspectives.Biomedicines · 2026Review
- Recent advances in pulmonary fibrosis: from lung surfactant to the immune connection.Respiratory research · 2026Review
- Research Advances in Therapeutic Strategies and Drug Delivery Systems for Pathological Scars.Pharmaceutics · 2026Review
- Mesenchymal Stem Cells-Derived Exosomes: Next-Generation Nanomedicines Toward Scarless Wound Healing.International journal of nanomedicine · 2026Review
- Research progress on scar-free healing.Annals of medicine · 2025Review
- Cloning and Expression ofAnimals : an open access journal from MDPI · 2025Article
- Wnt Activation in Mature Dermal Adipocytes Leads to Lipodystrophy and Skin Fibrosis via ATGL-Dependent Lipolysis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- SLC7A11 in Fibrosis: Molecular Mechanisms and Future Prospects.Aging and disease · 2025Review
- Dermal β-Catenin Is Required for Hedgehog-Driven Hair Follicle Neogenesis.The Journal of investigative dermatology · 2025Article
- Cytokine priming enhances the antifibrotic effects of human adipose derived mesenchymal stromal cells conditioned medium.Stem cell research & therapy · 2024Article
- Apical expansion of calvarial osteoblasts and suture patency is dependent on fibronectin cues.Development (Cambridge, England) · 2024Article
- Natural Compounds and Biomimetic Engineering to Influence Fibroblast Behavior in Wound Healing.International journal of molecular sciences · 2024Review
- Tissue fibrosis associated depletion of lipid-filled cells.Experimental dermatology · 2024Review
- Modulating embryonic signaling pathways paves the way for regeneration in wound healing.Frontiers in physiology · 2024Review
- Transformation of macrophages into myofibroblasts in fibrosis-related diseases: emerging biological concepts and potential mechanism.Frontiers in immunology · 2024Review
- The mechanism of gut-lung axis in pulmonary fibrosis.Frontiers in cellular and infection microbiology · 2024Review
- Hydrogel Loaded with Components for Therapeutic Applications in Hypertrophic Scars and Keloids.International journal of nanomedicine · 2024Review
- C-X-C domain ligand 14-mediated stromal cell-macrophage interaction as a therapeutic target for hand dermal fibrosis.Communications biology · 2023Article
- Unravelling morphoea aetiopathogenesis by next-generation sequencing of paired skin biopsies.Archives of dermatological research · 2023Article
- Macrophages and fibrosis: how resident and infiltrating mononuclear phagocytes account for organ injury, regeneration or atrophy.Frontiers in immunology · 2023Review
8 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Fibrosis is an end-stage response to tissue injury that is associated with loss of organ function as a result of excess extracellular matrix (ECM) production by fibroblasts. In skin, pathological fibrosis is evident during keloid scar formation, systemic sclerosis (SSc) and morphea. Dermal fibroblasts in these fibrotic diseases exhibit increased Wnt/β-catenin signalling, a pathway that is sufficient to cause fibrosis in mice. However, in the context of this complex pathology, the precise pro-fibrotic consequences of Wnt/β-catenin signalling are not known. We found that expression of stabilized β-catenin in mouse dermal fibroblasts resulted in spontaneous, progressive skin fibrosis with thickened collagen fibres and altered collagen fibril morphology. The fibrotic phenotype was predominated by resident dermal fibroblasts. Genome-wide profiling of the fibrotic mouse dermis revealed elevated expression of matrix-encoding genes, and the promoter regions of these genes were enriched for Tcf/Lef family transcription factor binding sites. Additionally, we identified 32 β-catenin-responsive genes in our mouse model that are also over-expressed in human fibrotic tissues and poised for regulation by Tcf/Lef family transcription factors. Therefore, we have uncovered a matrix-regulatory role for stabilized β-catenin in fibroblasts in vivo and have defined a set of β-catenin-responsive genes with relevance to fibrotic disease.
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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.