ArticleJCI insight2020
Distinctive lipid signatures of bronchial epithelial cells associated with cystic fibrosis drugs, including Trikafta.
Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 31 citations in OpenAlex.
- Rhinovirus infection promotes suppression of sphingosine and enhanced bacterial infection in cystic fibrosis airways.The Journal of biological chemistry · 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
- Insights on the Pathogenesis ofJournal of clinical medicine · 2025Review
- Mapping the oxidative landscape in cystic fibrosis: methodological frontiers and application.Frontiers in pharmacology · 2025Review
- Review
- The effect of triple CFTR modulator therapy and azithromycin on ion channels and inflammation in cystic fibrosis.ERJ open research · 2024Article
- Dysregulation of the Arachidonic Acid Pathway in Cystic Fibrosis: Implications for Chronic Inflammation and Disease Progression.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Sphingosine kills intracellular Pseudomonas aeruginosa and Staphylococcus aureus.Pathogens and disease · 2024Article
- Reduced Sphingosine in Cystic Fibrosis Increases Susceptibility toInternational journal of molecular sciences · 2023Article
- Elexacaftor-Tezacaftor-Ivacaftor: A Life-Changing Triple Combination of CFTR Modulator Drugs for Cystic Fibrosis.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Post-approval studies with the CFTR modulators Elexacaftor-Tezacaftor-Ivacaftor.Frontiers in pharmacology · 2023Review
- The fatty acid imbalance of cystic fibrosis exists at birth independent of feeding in pig and ferret models.Clinical science (London, England : 1979) · 2022Article
- Treatment With LAU-7b Complements CFTR Modulator Therapy by Improving Lung Physiology and Normalizing Lipid Imbalance Associated With CF Lung Disease.Frontiers in pharmacology · 2022Article
- New drugs in cystic fibrosis: what has changed in the last decade?Therapeutic advances in chronic disease · 2022Review
- Role for animal models in understanding essential fatty acid deficiency in cystic fibrosis.Cellular and molecular life sciences : CMLS · 2021Review
- Mechanistic analysis and significance of sphingomyelinase-mediated decreases in transepithelial CFTR currents in nHBEs.Physiological reports · 2021Article
- Partial Rescue of F508del-CFTR Stability and Trafficking Defects by Double Corrector Treatment.International journal of molecular sciences · 2021Article
- Is the ENaC Dysregulation in CF an Effect of Protein-Lipid Interaction in the Membranes?International journal of molecular sciences · 2021Review
- Dysfunctional Inflammation in Cystic Fibrosis Airways: From Mechanisms to Novel Therapeutic Approaches.International journal of molecular sciences · 2021Review
- Acid Ceramidase Rescues Cystic Fibrosis Mice from Pulmonary Infections.Infection and immunity · 2021Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In recent years, a number of drugs have been approved for the treatment of cystic fibrosis (CF). Among them, newly released Trikafta, a combination of 3 drugs (VX-661/VX-445/VX-770), holds great promise to radically improve the quality of life for a large portion of patients with CF carrying 1 copy of F508del, the most frequent CF transmembrane conductance regulator (CFTR) mutation. Currently available disease-modifying CF drugs work by rescuing the function of the mutated CFTR anion channel. Recent research has shown that membrane lipids, and the cell lipidome in general, play a significant role in the mechanism of CFTR-defective trafficking and, on the other hand, its rescue. In this paper, by using untargeted lipidomics on CFBE41o- cells, we identified distinctive changes in the bronchial epithelial cell lipidome associated with treatment with Trikafta and other CF drugs. Particularly interesting was the reduction of levels of ceramide, a known molecular player in the induction of apoptosis, which appeared to be associated with a decrease in the susceptibility of cells to undergo apoptosis. This evidence could account for additional beneficial roles of the triple combination of drugs on CF phenotypes.
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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.