ArticleAmerican journal of respiratory cell and molecular biology2014
IκBβ-mediated NF-κB activation confers protection against hyperoxic lung injury.
Article in American journal of respiratory cell and molecular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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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.
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Who cites it
15 citing papers in PubMed, 17 citations in OpenAlex.
- Prenatal lipopolysaccharide exposure programs the early-life lung development by modulating mesenchymal fibroblasts in a time- and dose-dependent manner.BMC medicine · 2025Article
- Endothelial-specific loss of IKKβ disrupts pulmonary endothelial angiogenesis and impairs postnatal lung growth.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Oxygen toxicity: cellular mechanisms in normobaric hyperoxia.Cell biology and toxicology · 2023Review
- APAP-Induced IκBβ/NFκB Signaling Drives Hepatic Il6 Expression and Associated Sinusoidal Dilation.Toxicological sciences : an official journal of the Society of Toxicology · 2022Article
- Pulmonary implications of acetaminophen exposures independent of hepatic toxicity.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- Auranofin-Mediated NRF2 Induction Attenuates Interleukin 1 Beta Expression in Alveolar Macrophages.Antioxidants (Basel, Switzerland) · 2021Article
- Sex-differences in LPS-induced neonatal lung injury.Scientific reports · 2019Article
- Toxic Acetaminophen Exposure Induces Distal Lung ER Stress, Proinflammatory Signaling, and Emphysematous Changes in the Adult Murine Lung.Oxidative medicine and cellular longevity · 2019Article
- NF-κB in Oxidative Stress.Current opinion in toxicology · 2018Article
- Differential sex-specific effects of oxygen toxicity in human umbilical vein endothelial cells.Biochemical and biophysical research communications · 2017Article
- Calcitonin gene-related peptide protects type II alveolar epithelial cells from hyperoxia-induced DNA damage and cell death.Experimental and therapeutic medicine · 2017Article
- Sex-specific differences in neonatal hyperoxic lung injury.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Absence of TNF-α enhances inflammatory response in the newborn lung undergoing mechanical ventilation.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Endotoxemia Induces IκBβ/NF-κB-Dependent Endothelin-1 Expression in Hepatic Macrophages.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Sustained hyperoxia-induced NF-κB activation improves survival and preserves lung development in neonatal mice.American journal of physiology. Lung cellular and molecular physiology · 2014Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Supplemental oxygen is frequently used in an attempt to improve oxygen delivery; however, prolonged exposure results in damage to the pulmonary endothelium and epithelium. Although NF-κB has been identified as a redox-responsive transcription factor, whether NF-κB activation exacerbates or attenuates hyperoxic lung injury is unclear. We determined that sustained NF-κB activity mediated by IκBβ attenuates lung injury and prevents mortality in adult mice exposed to greater than 95% O2. Adult wild-type mice demonstrated evidence of alveolar protein leak and 100% mortality by 6 days of hyperoxic exposure, and showed NF-κB nuclear translocation that terminated after 48 hours. Furthermore, these mice showed increased expression of NF-κB-regulated proinflammatory and proapoptotic cytokines. In contrast, mice overexpressing the NF-κB inhibitory protein, IκBβ (AKBI), demonstrated significant resistance to hyperoxic lung injury, with 50% surviving through 8 days of exposure. This was associated with NF-κB nuclear translocation that persisted through 96 hours of exposure. Although induction of NF-κB-regulated proinflammatory cytokines was not different between wild-type and AKBI mice, significant up-regulation of antiapoptotic proteins (BCL-2, BCL-XL) was found exclusively in AKBI mice. We conclude that sustained NF-κB activity mediated by IκBβ protects against hyperoxic lung injury through increased expression of antiapoptotic genes.
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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.