ArticleDiscovery medicine2010
The NF-kappaB signaling in cystic fibrosis lung disease: pathophysiology and therapeutic potential.
Article in Discovery medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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
42 citing papers in PubMed, 73 citations in OpenAlex.
- Effect of Ibuprofen on Markers of Acute Kidney Injury, Intestinal Injury, and Endotoxemia after Running in the Heat.Medicine and science in sports and exercise · 2025Trial
- Comparative Single-Cell Transcriptomics Uncovers Shared and Distinct Molecular Signatures in Cystic Fibrosis and Primary Ciliary Dyskinesia.bioRxiv : the preprint server for biology · 2025Article
- Revealing the impact ofFrontiers in immunology · 2025Article
- Loss of CFTR Reverses Senescence Hallmarks in SARS-CoV-2 Infected Bronchial Epithelial Cells.International journal of molecular sciences · 2024Article
- A review of pulmonary neutrophilia and insights into the key role of neutrophils in particle-induced pathogenesis in the lung from animal studies of lunar dusts and other poorly soluble dust particles.Critical reviews in toxicology · 2023Review
- Article
- Chasing a Breath of Fresh Air in Cystic Fibrosis (CF): Therapeutic Potential of Selective HDAC6 Inhibitors to Tackle Multiple Pathways in CF Pathophysiology.Journal of medicinal chemistry · 2022Review
- Airway Administration of Flagellin Regulates the Inflammatory Response toAmerican journal of respiratory cell and molecular biology · 2021Article
- SFPQ rescues F508del-CFTR expression and function in cystic fibrosis bronchial epithelial cells.Scientific reports · 2021Article
- Reduced neutrophil elastase inhibitor elafin and elevated transforming growth factor-βERJ open research · 2021Article
- Impairment in inflammasome signaling by the chronic Pseudomonas aeruginosa isolates from cystic fibrosis patients results in an increase in inflammatory response.Cell death & disease · 2021Article
- Prognosis-Based Early Intervention Strategies to Resolve Exacerbation and Progressive Lung Function Decline in Cystic Fibrosis.Journal of personalized medicine · 2021Article
- Are cystic fibrosis mutation carriers a potentially highly vulnerable group to COVID-19?Journal of cellular and molecular medicine · 2020Article
- Mutant CFTR Drives TWIST1 mediated epithelial-mesenchymal transition.Cell death & disease · 2020Article
- Review
- Is PI3K a Villain in Cystic Fibrosis?American journal of respiratory cell and molecular biology · 2020Article
- Considerations for Phage Therapy AgainstFrontiers in microbiology · 2020Review
- miR-135a Alleviates Silica-Induced Pulmonary Fibrosis by Targeting NF-Mediators of inflammation · 2020Article
- Transcriptional consequences of impaired immune cell responses induced by cystic fibrosis plasma characterized via dual RNA sequencing.BMC medical genomics · 2019Article
- Transcriptome Profiling and Molecular Therapeutic Advances in Cystic Fibrosis: Recent Insights.Genes · 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
2 authors at 1 institution in 1 country.
Funding
Abstract
Lung disease is the major cause of morbidity and mortality of cystic fibrosis (CF), an autosomal recessive disease caused by mutations in CF transmembrane-conductance regulator (CFTR) gene. In CF, elevated levels of interleukin-8 (IL-8) signaling mediated by the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappaB) result in chronic infection, neutrophilic inflammation, and progressive airway destruction. The most frequent mutation in the CFTR gene is the deletion of phenylalanine 508 (DeltaF508), which results in its endoplasmic reticulum associated degradation (ERAD) by the ubiquitin-proteasome system. The inability of DeltaF508-CFTR to reach cell surface leads to inherently high levels of NF-kappaB. Severity of CF lung disease depends on the levels of functional CFTR on cell surface that control its chloride transport and NF-kappaB mediated innate immune response functions. NF-kappaB mediated chronic inflammation is a prominent feature of CF lung disease and the mechanism(s) by which CFTR regulates these inflammatory signaling pathways is becoming apparent. Recent data suggest that CFTR localization to lipid-rafts is critical for regulating NF-kappaB mediated innate immune response and chronic CF lung disease. We anticipate that targeting the pathways, which facilitates CFTR's rescue to the cell surface and lipid-rafts, will not only restore CFTR channel function but also control NF-kappaB mediated chronic inflammation, although the level of correction may be a critical factor for therapeutic efficacy. We discuss here the mechanisms of NF-kappaB induction in CF, pathogenesis of CF lung disease, and novel therapeutic strategies that may help in reversing the chronic CF lung disease.
Indexed as
Identifiers
20423679PMC3114405W1587489068What 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.