ArticleThe Journal of clinical investigation2022
Losartan ameliorates TGF-β1-induced CFTR dysfunction and improves correction by cystic fibrosis modulator therapies.
Article in The Journal of clinical investigation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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.
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
11 citing papers in PubMed, 14 citations in OpenAlex.
- Jinshui Liujun Decoction attenuates cigarette smoke-induced small airway remodeling via the TGF-β/Smad2/CFTR Axis.The journal of physiological sciences : JPS · 2026Article
- Hypoxia-preconditioned bone marrow mesenchymal stem cell-derived exosomes ameliorate knee osteoarthritis by promoting cartilage regeneration and alleviating pain in rats.Regenerative therapy · 2026Article
- Oral losartan yields subtherapeutic airway exposure compared to nebulized delivery and fails to improve mucociliary clearance in cystic fibrosis.Frontiers in pharmacology · 2026Article
- Differential BK channel potentiation by vanzacaftor enantiomers enables therapy for modulator-ineligible people with cystic fibrosis.The Journal of clinical investigation · 2025Article
- TGF-β induces excessive pulmonary IL-6 secretion in cystic fibrosis via PI3K.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Cystic fibrosis.Nature reviews. Disease primers · 2024Review
- RUNX1 promotes liver fibrosis progression through regulating TGF-β signalling.International journal of experimental pathology · 2023Article
- Review
- Nebulized Menthol Impairs Mucociliary Clearance via TRPM8 and MUC5AC/MUC5B in Primary Airway Epithelial Cells.International journal of molecular sciences · 2023Article
- The CFTR Amplifier Nesolicaftor Rescues TGF-β1 Inhibition of Modulator-Corrected F508del CFTR Function.International journal of molecular sciences · 2022Article
- Vegetable glycerin e-cigarette aerosols cause airway inflammation and ion channel dysfunction.Frontiers in pharmacology · 2022Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Highly effective modulator therapies dramatically improve the prognosis for those with cystic fibrosis (CF). The triple combination of elexacaftor, tezacaftor, and ivacaftor (ETI) benefits many, but not all, of those with the most common F508del mutation in the CF transmembrane conductance regulator (CFTR). Here, we showed that poor sweat chloride concentration responses and lung function improvements upon initiation of ETI were associated with elevated levels of active TGF-β1 in the upper airway. Furthermore, TGF-β1 impaired the function of ETI-corrected F508del-CFTR, thereby increasing airway surface liquid (ASL) absorption rates and inducing mucus hyperconcentration in primary CF bronchial epithelial cells in vitro. TGF-β1 not only decreased CFTR mRNA, but was also associated with increases in the mRNA expression of TNFA and COX2 and TNF-α protein. Losartan improved TGF-β1-mediated inhibition of ETI-corrected F508del-CFTR function and reduced TNFA and COX2 mRNA and TNF-α protein expression. This likely occurred by improving correction of mutant CFTR rather than increasing its mRNA (without an effect on potentiation), thereby reversing the negative effects of TGF-β1 and improving ASL hydration in the CF airway epithelium in vitro. Importantly, these effects were independent of type 1 angiotensin II receptor inhibition.
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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.