ArticleAmerican journal of respiratory cell and molecular biology2011
Nuclear β-catenin is increased in systemic sclerosis pulmonary fibrosis and promotes lung fibroblast migration and proliferation.
Article in American journal of respiratory cell and molecular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.
What it found
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Who cites it
82 citing papers in PubMed, 151 citations in OpenAlex.
- Epithelial-mesenchymal transition in cutaneous fibrosis disease: from mechanisms to therapy.Frontiers in immunology · 2026Review
- Spatiotemporal analyses of the pan-cancer single-cell landscape reveal widespread profibrotic ecotypes associated with tumor immunity.Nature cancer · 2025Article
- Advances in the Molecular Mechanisms of Pulmonary Fibrosis in Systemic Sclerosis: A Comprehensive Review.International journal of molecular sciences · 2025Review
- Emerging therapies for the treatment of systemic sclerosis.Nature reviews. Rheumatology · 2025Review
- Emerging Concepts in Fibroblast Biology and Progressive Pulmonary Fibrosis.Seminars in respiratory and critical care medicine · 2025Review
- CasRx-based Wnt activation promotes alveolar regeneration while ameliorating pulmonary fibrosis in a mouse model of lung injury.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Histone Deacetylase 7-Derived 7-Amino Acid Peptide Increases Skin Wound Healing via Regulating Epidermal Fibroblast Proliferation and Migration.Journal of cellular and molecular medicine · 2024Article
- Tissue fibrosis associated depletion of lipid-filled cells.Experimental dermatology · 2024Review
- C-X-C domain ligand 14-mediated stromal cell-macrophage interaction as a therapeutic target for hand dermal fibrosis.Communications biology · 2023Article
- Involvement of Epithelial-Mesenchymal Transition (EMT) in Autoimmune Diseases.International journal of molecular sciences · 2023Review
- Unravelling morphoea aetiopathogenesis by next-generation sequencing of paired skin biopsies.Archives of dermatological research · 2023Article
- The inhibition of Wnt signaling attenuates RANKL-induced osteoclastogenic macrophage activation.Vascular biology (Bristol, England) · 2023Article
- First Characterization of the Transcriptome of Lung Fibroblasts of SSc Patients and Healthy Donors of African Ancestry.International journal of molecular sciences · 2023Article
- HIPK2 as a Novel Regulator of Fibrosis.Cancers · 2023Review
- The Molecular Mechanisms of Systemic Sclerosis-Associated Lung Fibrosis.International journal of molecular sciences · 2023Review
- Skin Fibrosis and Recovery Is Dependent on Wnt Activation via DPP4.The Journal of investigative dermatology · 2022Article
- Genome-wide DNA methylation pattern in systemic sclerosis microvascular endothelial cells: Identification of epigenetically affected key genes and pathways.Journal of scleroderma and related disorders · 2022Article
- A broad look into the future of systemic sclerosis.Therapeutic advances in musculoskeletal disease · 2022Review
- Effect of supercritical carbon dioxide fluid extract from Chrysanthemum indicum Linné on bleomycin-induced pulmonary fibrosis.BMC complementary medicine and therapies · 2021Article
- Long Noncoding RNAInternational journal of molecular sciences · 2021Article
22 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Pulmonary fibrosis is a disease that results in loss of normal lung architecture, but the signaling events that drive tissue destruction are incompletely understood. Wnt/β-catenin signaling is important in normal lung development, but whether abnormal signaling occurs in lung fibrosis due to systemic sclerosis and the consequences of β-catenin signaling toward the fibrogenic phenotype remain poorly defined. In this study, we show nuclear β-catenin accumulation in fibroblastic foci from lungs of patients with systemic sclerosis-associated advanced pulmonary fibrosis. Forced activation of β-catenin signaling in three independently derived sources of normal human lung fibroblasts promotes proliferation and migratory activities but is not sufficient to activate classic markers of fibroblast activation, such as TGF-β, type 1 collagen, α-smooth muscle actin, and connective tissue growth factor. These findings indicate that activation of β-catenin signaling in pulmonary fibroblasts may be a common feature of lung fibrosis, contributing to fibroproliferative and migratory activities associated with the 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.