ArticleRespiratory research2015
Conditional overexpression of TGFβ1 promotes pulmonary inflammation, apoptosis and mortality via TGFβR2 in the developing mouse lung.
Article in Respiratory research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 63 citations in OpenAlex.
- [Resveratrol increases sirtuin 1 expression in peripheral blood mononuclear cells of premature infants and inhibits the oxidative stress induced by hyperoxia in vivo].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2016Trial
- Murine models of pulmonary fibrosis: mechanisms, limitations and translational insights.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Bronchopulmonary dysplasia demonstrates dysregulated autotaxin/lysophosphatidic acid signaling in a neonatal mouse model.Pediatric research · 2025Article
- Article
- Impaired myofibroblast proliferation is a central feature of pathologic post-natal alveolar simplification.eLife · 2024Article
- Impaired Myofibroblast Proliferation is a Central Feature of Pathologic Post-Natal Alveolar Simplification.bioRxiv : the preprint server for biology · 2024Article
- Conditional knockout of ITGB4 in bronchial epithelial cells directs bronchopulmonary dysplasia.Journal of cellular and molecular medicine · 2023Article
- Toll-like receptor-guided therapeutic intervention of human cancers: molecular and immunological perspectives.Frontiers in immunology · 2023Review
- The Role of Insulin Receptor Substrate Proteins in Bronchopulmonary Dysplasia and Asthma: New Potential Perspectives.International journal of molecular sciences · 2022Review
- Association of immune cell recruitment and BPD development.Molecular and cellular pediatrics · 2022Review
- Specific epigenetic regulators serve as potential therapeutic targets in idiopathic pulmonary fibrosis.Heliyon · 2022Review
- TLR/WNT: A Novel Relationship in Immunomodulation of Lung Cancer.International journal of molecular sciences · 2022Review
- Amphibian-derived peptide homodimer OA-GL17d promotes skin wound regeneration through the miR-663a/TGF-β1/Smad axis.Burns & trauma · 2022Article
- Patho-mechanisms of the origins of bronchopulmonary dysplasia.Molecular and cellular pediatrics · 2021Review
- Hyperoxia-activated circulating extracellular vesicles induce lung and brain injury in neonatal rats.Scientific reports · 2021Article
- Single cell transcriptomic analysis of murine lung development on hyperoxia-induced damage.Nature communications · 2021Article
- Hyperoxia and Lungs: What We Have Learned From Animal Models.Frontiers in medicine · 2021Review
- Regulatory mechanism of NOV/CCN3 in the inflammation and apoptosis of lung epithelial alveolar cells upon lipopolysaccharide stimulation.Molecular medicine reports · 2020Article
- Hyperoxia causes miR199a-5p-mediated injury in the developing lung.Pediatric research · 2019Article
- TLRs in pulmonary diseases.Life sciences · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundEarlier studies have reported that transforming growth factor beta 1(TGFβ1) is a critical mediator of hyperoxia-induced acute lung injury (HALI) in developing lungs, leading to impaired alveolarization and a pulmonary phenotype of bronchopulmonary dysplasia (BPD). However, the mechanisms responsible for the TGFβ1-induced inflammatory signals that lead to cell death and abnormal alveolarization are poorly understood. We hypothesized that TGFβ1 signaling via TGFβR2 is necessary for the pathogenesis of the BPD pulmonary phenotype resulting from HALI.
methodsWe utilized lung epithelial cell-specific TGFβ1 overexpressing transgenic and TGFβR2 null mutant mice to evaluate the effects on neonatal mortality as well as pulmonary inflammation and apoptosis in developing lungs. Lung morphometry was performed to determine the impaired alveolarization and multicolor flow cytometry studies were performed to detect inflammatory macrophages and monocytes in lungs. Apoptotic cell death was measured with TUNEL assay, immunohistochemistry and western blotting and protein expression of angiogenic mediators were also analyzed.
resultsOur data reveals that increased TGFβ1 expression in newborn mice lungs leads to increased mortality, macrophage and immature monocyte infiltration, apoptotic cell death specifically in Type II alveolar epithelial cells (AECs), impaired alveolarization, and dysregulated angiogenic molecular markers.
conclusionsOur study has demonstrated the potential role of inhibition of TGFβ1 signaling via TGFβR2 for improved survival, reduced inflammation and apoptosis that may provide insights for the development of potential therapeutic strategies targeted against HALI and BPD.
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.