ReviewBirth defects research. Part A, Clinical and molecular teratology2014
Nuclear factor-kappa-B signaling in lung development and disease: one pathway, numerous functions.
Review in Birth defects research. Part A, Clinical and molecular teratology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 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
70 citing papers in PubMed, 106 citations in OpenAlex.
- Impact of Gestational Maternal SARS-CoV-2 Infection on Neonatal Inflammatory Biomarkers.American journal of reproductive immunology (New York, N.Y. : 1989) · 2026Article
- Tracheal aspirates of mechanically ventilated preterm infants possess cytopathic tau variants: a prospective exploratory study.American journal of physiology. Lung cellular and molecular physiology · 2026Article
- Prediction of primary human targets and toxicity mechanisms of imidacloprid using integrativeToxicology reports · 2026Article
- Umbilical cord blood cell transcriptional and methylation signatures at birth are associated with BPD development and chorioamnionitis: a pilot study.Scientific reports · 2026Article
- The potential role of CD44+ monocytes in mediating hyperinflammatory response in bronchopulmonary dysplasia in very premature infants.Pediatric research · 2026Article
- Peroxiredoxin 1 mediates bleomycin-induced acute lung injury in mice via macrophage NOD1/NF-κB axis.Respiratory research · 2026Article
- Macrophage Phenotypic Plasticity and Inflammatory Mechanisms in Hyperoxia-Induced Lung Injury.Journal of inflammation research · 2026Review
- The Inflammatory Nexus of Bronchopulmonary Dysplasia: From Molecular Pathways to Precision Therapeutics.Mediators of inflammation · 2026Review
- Impact of Gestational Maternal SARS-CoV-2 Infection on Neonatal Inflammatory Biomarkers.Research square · 2025Article
- Neutrophil-derived extracellular vesicles in the plasma of alpha-1 antitrypsin deficient individuals reveal pro-inflammatory metabolic and transcriptomic signatures.Extracellular vesicle · 2025Article
- Umbilical Cord Blood Cell Transcriptional and Methylation Signatures at Birth Are Associated with BPD Development.bioRxiv : the preprint server for biology · 2025Article
- Yes-associated protein induces age-dependent inflammatory signaling in the pulmonary endothelium.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Spatial and Temporal Expression Patterns of EDA2R, PCDH9, and TRAF7 inInternational journal of molecular sciences · 2025Article
- Yes-associated Protein Induces Age-dependent Inflammatory Signaling in the Pulmonary Endothelium.bioRxiv : the preprint server for biology · 2025Article
- The lung microvasculature promotes alveolar type 2 cell differentiation via secreted SPARCL1.Stem cell reports · 2025Article
- Identification and Functional Analysis of Key microRNAs in the Early Extrauterine Environmental Adaptation of Piglets.International journal of molecular sciences · 2025Article
- Rutin attenuates bleomycin-induced acute lung injuryFrontiers in pharmacology · 2025Article
- iRhom2 deficiency reduces sepsis-induced mortality associated with the attenuation of lung macrophages in mice.Histochemistry and cell biology · 2024Article
- Article
- Effect and mechanism of transient receptor potential canonical channel 3 on hyperoxic lung injury in neonatal rats.Pediatric discovery · 2024Article
10 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
In contrast to other organs, the lung completes a significant portion of its development after term birth. During this stage of alveolarization, division of the alveolar ducts into alveolar sacs by secondary septation, and expansion of the pulmonary vasculature by means of angiogenesis markedly increase the gas exchange surface area of the lung. However, postnatal completion of growth renders the lung highly susceptible to environmental insults such as inflammation that disrupt this developmental program. This is particularly evident in the setting of preterm birth, where impairment of alveolarization causes bronchopulmonary dysplasia, a chronic lung disease associated with significant morbidity. The nuclear factor κ-B (NFκB) family of transcription factors are ubiquitously expressed, and function to regulate diverse cellular processes including proliferation, survival, and immunity. Extensive evidence suggests that activation of NFκB is important in the regulation of inflammation and in the control of angiogenesis. Therefore, NFκB-mediated downstream effects likely influence the lung response to injury and may also mediate normal alveolar development. This review summarizes the main biologic functions of NFκB, and highlights the regulatory mechanisms that allow for diversity and specificity in downstream gene activation. This is followed by a description of the pro and anti-inflammatory functions of NFκB in the lung, and of NFκB-mediated angiogenic effects. Finally, this review summarizes the clinical and experimental data that support a role for NFκB in mediating postnatal angiogenesis and alveolarization, and discusses the challenges that remain in developing therapies that can selectively block the detrimental functions of NFκB yet preserve the beneficial effects.
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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.