ArticleAmerican journal of respiratory and critical care medicine2014
Wnt coreceptor Lrp5 is a driver of idiopathic pulmonary fibrosis.
Article in American journal of respiratory and critical care medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
66 citing papers in PubMed, 108 citations in OpenAlex.
- BCL9 inhibition promotes fibroblast lipogenesis by regulating macrophage-fibroblast interactions to attenuate pulmonary fibrosis.Signal transduction and targeted therapy · 2026Article
- C/EBPγ interacts with C/EBPα and activates the β-catenin pathway in idiopathic pulmonary fibrosis.Cellular and molecular life sciences : CMLS · 2026Article
- 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
- Engineerable mesenchymal stem cell-derived extracellular vesicles as promising therapeutic strategies for pulmonary fibrosis.Stem cell research & therapy · 2025Review
- MiR-148a-3p Loaded Human Umbilical Cord Mesenchymal Stem Cell-Derived Extracellular Vesicles Alleviates Silica-Induced Pulmonary Fibrosis by Inhibiting β-Catenin Signaling.International journal of nanomedicine · 2025Article
- A polymorphism in the FAM13A gene confers protection against tuberculosis in Brazilian workers exposed to silica.Jornal brasileiro de pneumologia : publicacao oficial da Sociedade Brasileira de Pneumologia e Tisilogia · 2025Article
- Immunobiology of pulmonary fibrosis.Frontiers in immunology · 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
- A WNT mimetic with broad spectrum FZD-specificity decreases fibrosis and improves function in a pulmonary damage model.Respiratory research · 2024Article
- Tissue fibrosis associated depletion of lipid-filled cells.Experimental dermatology · 2024Review
- TGF-β1, pSmad-2/3, Smad-7, and β-Catenin Are Augmented in the Pulmonary Arteries from Patients with Idiopathic Pulmonary Fibrosis (IPF): Role in Driving Endothelial-to-Mesenchymal Transition (EndMT).Journal of clinical medicine · 2024Article
- Listen to the WNT; It Talks: WNT7A Drives Epithelial-Mesenchymal Cross-Talk within the Fibrotic Niche in Idiopathic Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2023Article
- Basal Cell-derived WNT7A Promotes Fibrogenesis at the Fibrotic Niche in Idiopathic Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2023Article
- Plasticity towards Rigidity: A Macrophage Conundrum in Pulmonary Fibrosis.International journal of molecular sciences · 2022Review
- The Role of PTEN in Epithelial-Mesenchymal Transition.Cancers · 2022Review
- Matrix Metalloproteinases and Their Inhibitors in Pulmonary Fibrosis: EMMPRIN/CD147 Comes into Play.International journal of molecular sciences · 2022Review
- Dynamic Involvement of Telocytes in Modulating Multiple Signaling Pathways in Cardiac Cytoarchitecture.International journal of molecular sciences · 2022Review
- Research Progress in the Molecular Mechanisms, Therapeutic Targets, and Drug Development of Idiopathic Pulmonary Fibrosis.Frontiers in pharmacology · 2022Review
- Noncanonical Wnt Signaling Promotes Myofibroblast Differentiation in Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2021Article
- Endothelial-to-mesenchymal transition in systemic sclerosis.Clinical and experimental immunology · 2021Review
6 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
rationaleWnt/β-catenin signaling has been implicated in lung fibrosis, but how this occurs and whether expression changes in Wnt pathway components predict disease progression is unknown.
objectivesTo determine whether the Wnt coreceptor Lrp5 drives pulmonary fibrosis in mice and is predictive of disease severity in humans.
methodsWe examined mice with impaired Wnt signaling caused by loss of the Wnt coreceptor Lrp5 in models of lung fibrosis induced by bleomycin or an adenovirus encoding an active form of transforming growth factor (TGF)-β. We also analyzed gene expression in peripheral blood mononuclear cells (PBMC) from patients with idiopathic pulmonary fibrosis (IPF). MEASUREMENTS AND MAIN
resultsIn patients with IPF, analysis of peripheral blood mononuclear cells revealed that elevation of positive regulators, Lrp5 and 6, was independently associated with disease progression. LRP5 was also associated with disease severity at presentation in an additional cohort of patients with IPF. Lrp5 null mice were protected against bleomycin-induced pulmonary fibrosis, an effect that was phenocopied by direct inhibition of β-catenin signaling by the small molecular inhibitor of β-catenin responsive transcription. Transplantation of Lrp5 null bone marrow cells into wild-type mice did not limit fibrosis. Instead, Lrp5 loss was associated with reduced TGF-β production by alveolar type 2 cells and leukocytes. Consistent with a role of Lrp5 in the activation of TGF-β, Lrp5 null mice were not protected against lung fibrosis induced by TGF-β.
conclusionsWe show that the Wnt coreceptor, Lrp5, is a genetic driver of lung fibrosis in mice and a marker of disease progression and severity in humans with IPF. Evidence that TGF-β signaling can override a loss in Lrp5 has implications for patient selection and timing of Wnt pathway inhibitors in lung fibrosis.
Indexed as
Identifiers
What OpenQuestion holds
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.