ArticleHuman molecular genetics2019
Impact of Fgf10 deficiency on pulmonary vasculature formation in a mouse model of bronchopulmonary dysplasia.
Article in Human molecular genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 2 of them syntheses that pooled it.
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Who cites it
26 citing papers in PubMed, 2 syntheses or guidelines pooled it, 35 citations in OpenAlex.
- Hyperoxia and pulmonary vascular injury in bronchopulmonary dysplasia: pathogenic mechanisms and emerging therapies-a systematic review.Pediatric research · 2026Pooled it
- Phenotypic spectrum ofPeerJ · 2022Pooled it
- Review
- Frameshift Mutations in Exon 1 ofJournal of developmental biology · 2026Article
- FGF family in health and disease.Molecular biomedicine · 2026Review
- Caffeine Protects Against Hyperoxia-Induced Structural Lung Injury and Restores Alveolar Development in Neonatal Rats.Antioxidants (Basel, Switzerland) · 2025Article
- Morphological and molecular aspects of lung development.Histology and histopathology · 2025Review
- Sex-biased human thymic architecture guides T cell development through spatially defined niches.Developmental cell · 2025Article
- Reinitiating lung development: a novel approach in the management of bronchopulmonary dysplasia.Respiratory research · 2024Review
- Anti-CCL2 therapy reduces oxygen toxicity to the immature lung.Cell death discovery · 2024Article
- Implications in Cancer of Nuclear Micro RNAs, Long Non-Coding RNAs, and Circular RNAs Bound by PRC2 and FUS.Cancers · 2024Review
- Stem/Progenitor Cells and Related Therapy in Bronchopulmonary Dysplasia.International journal of molecular sciences · 2023Review
- Prophylactic Administration of Mesenchymal Stromal Cells Does Not Prevent Arrested Lung Development in Extremely Premature-Born Non-Human Primates.Stem cells translational medicine · 2023Article
- Insights into the Black Box of Intra-Amniotic Infection and Its Impact on the Premature Lung: From Clinical and Preclinical Perspectives.International journal of molecular sciences · 2022Review
- TRAIL protects the immature lung from hyperoxic injury.Cell death & disease · 2022Article
- New developments in the biology of fibroblast growth factors.WIREs mechanisms of disease · 2022Review
- FGF10 Triggers De Novo Alveologenesis in a Bronchopulmonary Dysplasia Model: Impact on Resident Mesenchymal Niche Cells.Stem cells (Dayton, Ohio) · 2022Article
- When inflammation meets lung development-an update on the pathogenesis of bronchopulmonary dysplasia.Molecular and cellular pediatrics · 2022Review
- Lung epithelium development and airway regeneration.Frontiers in cell and developmental biology · 2022Review
- Early Changes and Indicators Characterizing Lung Aging in Neonatal Chronic Lung Disease.Frontiers in medicine · 2021Review
Corrections and comments
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Authors and funding
18 authors at 7 institutions in 4 countries.
Funding
Abstract
Bronchopulmonary dysplasia (BPD), characterized by alveoli simplification and dysmorphic pulmonary microvasculature, is a chronic lung disease affecting prematurely born infants. Pulmonary hypertension (PH) is an important BPD feature associated with morbidity and mortality. In human BPD, inflammation leads to decreased fibroblast growth factor 10 (FGF10) expression but the impact on the vasculature is so far unknown. We used lungs from Fgf10+/- versus Fgf10+/+ pups to investigate the effect of Fgf10 deficiency on vascular development in normoxia (NOX) and hyperoxia (HOX, BPD mouse model). To assess the role of fibroblast growth factor receptor 2b (Fgfr2b) ligands independently of early developmentaldefects, we used an inducible double transgenic system in mice allowing inhibition of Fgfr2b ligands activity. Using vascular morphometry, we quantified the pathological changes. Finally, we evaluated changes in FGF10, surfactant protein C (SFTPC), platelet endothelial cell adhesion molecule (PECAM) and alpha-smooth muscle actin 2 (α-SMA) expression in human lung samples from patients suffering from BPD. In NOX, no major difference in the lung vasculature between Fgf10+/- and control pups was detected. In HOX, a greater loss of blood vessels in Fgf10+/- lungs is associated with an increase of poorly muscularized vessels. Fgfr2b ligands inhibition postnatally in HOX is sufficient to decrease the number of blood vessels while increasing the level of muscularization, suggesting a PH phenotype. BPD lungs exhibited decreased FGF10, SFTPC and PECAM but increased α-SMA. Fgf10 deficiency-associated vascular defects are enhanced in HOX and could represent an additional cause of morbidity in human patients with BPD.
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Registered trials
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