ArticleThe Journal of experimental medicine2017
Noncanonical WNT-5A signaling impairs endogenous lung repair in COPD.
Article in The Journal of experimental medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 112 papers.
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Who cites it
112 citing papers in PubMed, 193 citations in OpenAlex.
- Transcriptomic landscape of airway epithelial repair: Contrasting acute and chronic injury in mustard lung and COPD.Journal, genetic engineering & biotechnology · 2026Article
- Novel netrin-1-Unc5b-Klf4 axis balances AT2 survival in experimental bronchopulmonary dysplasia.American journal of respiratory cell and molecular biology · 2026Article
- Extracellular vesicles in senescence-associated chronic lung diseases.Chinese medical journal · 2026Review
- Concerted action of gammaherpesvirus infection and moderate hyperoxia on lung structural development including effects on critical lung fibroblast functions in neonatal mice.Molecular and cellular pediatrics · 2026Article
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- Construction of Rheumatoid Arthritis-Associated Interstitial Lung Disease diagnostic model and identification of biomarkers based on a multi-omics integration strategy of machine learning.Clinics (Sao Paulo, Brazil) · 2026Article
- Exploring the Roles of Wnt Signaling Pathway and Non-Coding RNAs in COPD.International journal of chronic obstructive pulmonary disease · 2026Review
- Breaking barriers in pulmonary health of patients with metabolic diseases: senolytics and beyond.Frontiers in aging · 2026Review
- Temporal regulation of wnt signaling in alveolar development and regeneration: mechanistic insights and therapeutic advances in chronic lung diseases.Frontiers in cell and developmental biology · 2026Review
- Wnt signaling pathway in lung aging and aging-related chronic lung diseases.Biogerontology · 2025Review
- Fzd2 orchestrates canonical and non-canonical Wnt signaling to regulate lung development and fibrosis.Cell communication and signaling : CCS · 2025Article
- Mechanistic Insights and Therapeutic Potential of Wnt5a Signaling in Alveolar Epithelial Cell Development and Bronchopulmonary Dysplasia.Stem cell reviews and reports · 2025Review
- Post-COPD: Can Emphysema Be Repaired?American journal of respiratory and critical care medicine · 2025Article
- Engineerable mesenchymal stem cell-derived extracellular vesicles as promising therapeutic strategies for pulmonary fibrosis.Stem cell research & therapy · 2025Review
- Mechanisms and markers of lung ageing in health and disease.European respiratory review : an official journal of the European Respiratory Society · 2025Review
- Influenza virus-induced type I interferons disrupt alveolar epithelial repair and tight junction integrity in the developing lung.Mucosal immunology · 2025Article
- Non-canonical Wnt signaling promotes epithelial fluidization in the repairing airway.Nature communications · 2025Article
- Compound screening in human airway basal cells identifies Wnt pathway activators as potential pro-regenerative therapies.Journal of cell science · 2025Article
- Bone Marrow Mesenchymal Stem Cells-Derived Exosomes Inhibit Apoptosis of Pulmonary Microvascular Endothelial Cells in COPD Mice Through miR-30b/Wnt5a Pathway.International journal of nanomedicine · 2025Article
52 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
16 authors at 5 institutions in 4 countries.
Funding
Abstract
Chronic obstructive pulmonary disease (COPD) is a leading cause of death worldwide. One main pathological feature of COPD is the loss of functional alveolar tissue without adequate repair (emphysema), yet the underlying mechanisms are poorly defined. Reduced WNT-β-catenin signaling is linked to impaired lung repair in COPD; however, the factors responsible for attenuating this pathway remain to be elucidated. Here, we identify a canonical to noncanonical WNT signaling shift contributing to COPD pathogenesis. We demonstrate enhanced expression of noncanonical WNT-5A in two experimental models of COPD and increased posttranslationally modified WNT-5A in human COPD tissue specimens. WNT-5A was increased in primary lung fibroblasts from COPD patients and induced by COPD-related stimuli, such as TGF-β, cigarette smoke (CS), and cellular senescence. Functionally, mature WNT-5A attenuated canonical WNT-driven alveolar epithelial cell wound healing and transdifferentiation in vitro. Lung-specific WNT-5A overexpression exacerbated airspace enlargement in elastase-induced emphysema in vivo. Accordingly, inhibition of WNT-5A in vivo attenuated lung tissue destruction, improved lung function, and restored expression of β-catenin-driven target genes and alveolar epithelial cell markers in the elastase, as well as in CS-induced models of COPD. We thus identify a novel essential mechanism involved in impaired mesenchymal-epithelial cross talk in COPD pathogenesis, which is amenable to therapy.
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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.