ReviewMolecules (Basel, Switzerland)2022
Cystic Fibrosis and Oxidative Stress: The Role of CFTR.
Review in Molecules (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
32 citing papers in PubMed, 47 citations in OpenAlex.
- CFTR regulates lipid metabolism by relieving adipose inflammation in obesity.International journal of obesity (2005) · 2026Article
- Jinshui Liujun Decoction attenuates cigarette smoke-induced small airway remodeling via the TGF-β/Smad2/CFTR Axis.The journal of physiological sciences : JPS · 2026Article
- Mucoactive Agents in Muco-Obstructive Lung Diseases: A Critical Reappraisal of Pharmacological Effects and Clinical Outcomes.Pharmaceuticals (Basel, Switzerland) · 2026Review
- PM2.5 toxin benzo[a]pyrene induces life-limiting inflammation and oxidative stress in the airway by up-regulation of TRPC6 and inactivation of β2AR/CFTR signaling.bioRxiv : the preprint server for biology · 2026Article
- Adaptation of Burkholderia cenocepacia to low oxygen drives changes consistent with adaptation to chronic infection.BMC microbiology · 2026Article
- Alteplase and Angioedema: Can Clinical Exome Sequencing Redefine the Paradigm?Life (Basel, Switzerland) · 2026Article
- Deciphering the role of the Sch9 serine/threonine kinase inFrontiers in fungal biology · 2026Article
- Impact of overexpression of wild-type CFTR and elexacaftor-tezacaftor-ivacaftor on oxylipin production by the CFBE41o- bronchial epithelial cell line.Prostaglandins & other lipid mediators · 2025Article
- Therapeutic Applications and Mechanisms of Superoxide Dismutase (SOD) in Different Pathogenesis.Biomolecules · 2025Review
- Redox Imbalance in Cystic Fibrosis: The Multifaceted Role of Oxidative Stress.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Decoding the role of extracellular vesicles in pathogenesis of cystic fibrosis.Molecular and cellular pediatrics · 2025Review
- Review
- Increased NFAT and NFκB signalling contribute to the hyperinflammatory phenotype in response to Aspergillus fumigatus in a mouse model of cystic fibrosis.PLoS pathogens · 2025Article
- Body composition changes and clinical outcomes in pediatric cystic fibrosis during 24 months of lumacaftor ivacaftor therapy based on real-world data.Scientific reports · 2025Observational
- Mapping the oxidative landscape in cystic fibrosis: methodological frontiers and application.Frontiers in pharmacology · 2025Review
- Identification of Novel Modifier Genes Associated With Pain in Cystic Fibrosis: An In Silico Gene Discovery.Human mutation · 2025Article
- Ivacaftor attenuates gentamicin-induced ototoxicity through the CFTR-Nrf2-HO1/NQO1 pathway.Redox report : communications in free radical research · 2024Article
- Genome-wide association study of susceptibility toThe European respiratory journal · 2024Article
- Update on the Role of β2AR and TRPV1 in Respiratory Diseases.International journal of molecular sciences · 2024Review
- A New Frontier in Cystic Fibrosis Pathophysiology: How and When Clock Genes Can Affect the Inflammatory/Immune Response in a Genetic Disease Model.Current issues in molecular biology · 2024Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
There is substantial evidence in the literature that patients with cystic fibrosis (CF) have higher oxidative stress than patients with other diseases or healthy subjects. This results in an increase in reactive oxygen species (ROS) and in a deficit of antioxidant molecules and plays a fundamental role in the progression of chronic lung damage. Although it is known that recurrent infection-inflammation cycles in CF patients generate a highly oxidative environment, numerous clinical and preclinical studies suggest that the airways of a patient with CF present an inherently abnormal proinflammatory milieu due to elevated oxidative stress and abnormal lipid metabolism even before they become infected. This could be directly related to cystic fibrosis transmembrane conductance regulator (CFTR) deficiency, which appears to produce a redox imbalance in epithelial cells and extracellular fluids. This review aims to summarize the main mechanism by which CFTR deficiency is intrinsically responsible for the proinflammatory environment that characterizes the lung of a patient with CF.
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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.