ArticleThe American journal of pathology2018
A Shared Pattern of β-Catenin Activation in Bronchopulmonary Dysplasia and Idiopathic Pulmonary Fibrosis.
Article in The American journal of pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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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
25 citing papers in PubMed, 44 citations in OpenAlex.
- A spatial transcriptomic atlas of acute neonatal lung injury across development and disease severity.bioRxiv : the preprint server for biology · 2025Article
- Cyclin G1 Regulates the Alveolarization in Models of Bronchopulmonary Dysplasia by Inhibiting AT2 Cell Proliferation.Biomolecules · 2025Article
- Editorial: Cellular and molecular mechanisms of lung regeneration, repair, and fibrosis, volume II.Frontiers in cell and developmental biology · 2025Article
- The transcriptomic signature of respiratory sensitizers using an alveolar model.Cell biology and toxicology · 2024Article
- A WNT mimetic with broad spectrum FZD-specificity decreases fibrosis and improves function in a pulmonary damage model.Respiratory research · 2024Article
- Epithelial Yap/Taz are required for functional alveolar regeneration following acute lung injury.JCI insight · 2023Article
- Hyperoxia exposure upregulates Dvl-1 and activates Wnt/β-catenin signaling pathway in newborn rat lung.BMC molecular and cell biology · 2023Article
- GSDMD deficiency ameliorates hyperoxia-induced BPD and ROP in neonatal mice.Scientific reports · 2023Article
- Genetic and Epidemiological Similarities, and Differences Between Postoperative Intraperitoneal Adhesion Development and Other Benign Fibro-proliferative Disorders.Reproductive sciences (Thousand Oaks, Calif.) · 2022Review
- The benefits, limitations and opportunities of preclinical models for neonatal drug development.Disease models & mechanisms · 2022Review
- Maladaptive functional changes in alveolar fibroblasts due to perinatal hyperoxia impair epithelial differentiation.JCI insight · 2022Article
- A Preconception Paternal Fish Oil Diet Prevents Toxicant-Driven New Bronchopulmonary Dysplasia in Neonatal Mice.Toxics · 2021Article
- Regenerative Medicine and the Hope for a Cure.Clinics in chest medicine · 2021Review
- Wnt signaling in lung development, regeneration, and disease progression.Communications biology · 2021Review
- WNT Signalling in Lung Physiology and Pathology.Handbook of experimental pharmacology · 2021Article
- Early Changes and Indicators Characterizing Lung Aging in Neonatal Chronic Lung Disease.Frontiers in medicine · 2021Review
- The self-fulfilling prophecy of pulmonary fibrosis: a selective inspection of pathological signalling loops.The European respiratory journal · 2020Review
- Review
- Hyperoxia Injury in the Developing Lung Is Mediated by Mesenchymal Expression of Wnt5A.American journal of respiratory and critical care medicine · 2020Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
Wnt/β-catenin signaling is necessary for normal lung development, and abnormal Wnt signaling contributes to the pathogenesis of both bronchopulmonary dysplasia (BPD) and idiopathic pulmonary fibrosis (IPF), fibrotic lung diseases that occur during infancy and aging, respectively. Using a library of human normal and diseased human lung samples, we identified a distinct signature of nuclear accumulation of β-catenin phosphorylated at tyrosine 489 and epithelial cell cytosolic localization of β-catenin phosphorylated at tyrosine 654 in early normal lung development and fibrotic lung diseases BPD and IPF. Furthermore, this signature was recapitulated in murine models of BPD and IPF. Image analysis of immunofluorescence colocalization demonstrated a consistent pattern of elevated nuclear phosphorylated β-catenin in the lung epithelium and surrounding mesenchyme in BPD and IPF, closely resembling the pattern observed in 18-week fetal lung. Nuclear β-catenin phosphorylated at tyrosine 489 associated with an increased expression of Wnt target gene AXIN2, suggesting that the observed β-catenin signature is of functional significance during normal development and injury repair. The association of specific modifications of β-catenin during normal lung development and again in response to lung injury supports the widely held concept that repair of lung injury involves the recapitulation of developmental programs. Furthermore, these observations suggest that β-catenin phosphorylation has potential as a therapeutic target for the treatment and prevention of both BPD and IPF.
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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.