ReviewFrontiers in medicine2015
The Extracellular Matrix in Bronchopulmonary Dysplasia: Target and Source.
Review in Frontiers in medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 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.
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Who cites it
55 citing papers in PubMed, 98 citations in OpenAlex.
- Sex-specific modulation of lung function and transcriptome in neonate mice exposed to thirdhand electronic-cigarette aerosols.Pediatric research · 2026Article
- What Does Next-Generation Mass Spectrometry Offer for Proteomics? A Comprehensive Platform Comparison.Journal of proteome research · 2026Article
- Label-free optical fingerprints of hyperoxia-induced lung alterations in preterm rabbits.Respiratory research · 2026Article
- Non-invasive respiratory support attenuates lung damage in a murine model of bronchopulmonary dysplasia.Frontiers in pediatrics · 2026Article
- Predicting Future Respiratory Hospitalizations in Extremely Premature Neonates Using Transcriptomic Data and Machine Learning.Children (Basel, Switzerland) · 2025Article
- The Impact of Antenatal and Postnatal Factors on the Development of the Pulmonary Microvasculature in Preterm Infants.Children (Basel, Switzerland) · 2025Article
- Interleukin-11 Is Involved in Hyperoxia-induced Bronchopulmonary Dysplasia in Newborn Mice by Mediating Epithelium-Fibroblast Cross-talk.Inflammation · 2025Article
- Unique Patterns of Circulating Extracellular Vesicles in Preterm Infants During Adaptation to Extra-Uterine Life.Journal of extracellular vesicles · 2025Observational
- 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
- Fetal origin of bronchopulmonary dysplasia: contribution of intrauterine inflammation.Molecular medicine (Cambridge, Mass.) · 2024Review
- Dynamic Hippo pathway activity underlies mesenchymal differentiation during lung alveolar morphogenesis.Development (Cambridge, England) · 2024Article
- Tenascin-C modulates alveolarization in bronchopulmonary dysplasia.Inflammation and regeneration · 2024Article
- Collagen type IV alpha 1 chain (COL4A1) expression in the developing human lung.BMC pulmonary medicine · 2024Article
- In vivo protein turnover rates in varying oxygen tensions nominate MYBBP1A as a mediator of the hyperoxia response.Science advances · 2023Article
- Prenatal vitamin D supplementation mitigates inflammation-related alveolar remodeling in neonatal mice.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Article
- Stretch regulates alveologenesis and homeostasis via mesenchymal Gαq/11-mediated TGFβ2 activation.Development (Cambridge, England) · 2023Article
- SOX2 and SOX21 in Lung Epithelial Differentiation and Repair.International journal of molecular sciences · 2022Review
- CircRNA, lncRNA, and mRNA profiles of umbilical cord blood exosomes from preterm newborns showing bronchopulmonary dysplasia.European journal of pediatrics · 2022Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bronchopulmonary dysplasia (BPD) is a common complication of preterm birth that contributes significantly to morbidity and mortality in neonatal intensive care units. BPD results from life-saving interventions, such as mechanical ventilation and oxygen supplementation used to manage preterm infants with acute respiratory failure, which may be complicated by pulmonary infection. The pathogenic pathways driving BPD are not well-delineated but include disturbances to the coordinated action of gene expression, cell-cell communication, physical forces, and cell interactions with the extracellular matrix (ECM), which together guide normal lung development. Efforts to further delineate these pathways have been assisted by the use of animal models of BPD, which rely on infection, injurious mechanical ventilation, or oxygen supplementation, where histopathological features of BPD can be mimicked. Notable among these are perturbations to ECM structures, namely, the organization of the elastin and collagen networks in the developing lung. Dysregulated collagen deposition and disturbed elastin fiber organization are pathological hallmarks of clinical and experimental BPD. Strides have been made in understanding the disturbances to ECM production in the developing lung, but much still remains to be discovered about how ECM maturation and turnover are dysregulated in aberrantly developing lungs. This review aims to inform the reader about the state-of-the-art concerning the ECM in BPD, to highlight the gaps in our knowledge and current controversies, and to suggest directions for future work in this exciting and complex area of lung development (patho)biology.
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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.