ArticleFree radical biology & medicine2012
CFTR is the primary known apical glutathione transporter involved in cigarette smoke-induced adaptive responses in the lung.
Article in Free radical biology & medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- Circulating biomarkers of antioxidant status and oxidative stress in people with cystic fibrosis: A systematic review and meta-analysis.Redox biology · 2020Pooled it
- Cellular Compartmentalization, Glutathione Transport and Its Relevance in Some Pathologies.Antioxidants (Basel, Switzerland) · 2023Review
- Combined Antioxidant, Anti-inflammaging and Mesenchymal Stem Cell Treatment: A Possible Therapeutic Direction in Elderly Patients with Chronic Obstructive Pulmonary Disease.Aging and disease · 2020Review
- Functional and metabolic impairment in cigarette smoke-exposed macrophages is tied to oxidative stress.Scientific reports · 2019Article
- Review
- Aberrant GSH reductase and NOX activities concur with defective CFTR to pro-oxidative imbalance in cystic fibrosis airways.Journal of bioenergetics and biomembranes · 2018Article
- The EGFR-ADAM17 Axis in Chronic Obstructive Pulmonary Disease and Cystic Fibrosis Lung Pathology.Mediators of inflammation · 2018Review
- Human Cellular Models for the Investigation of Lung Inflammation and Mucus Production in Cystic Fibrosis.Analytical cellular pathology (Amsterdam) · 2018Review
- Influenza virus infection alters ion channel function of airway and alveolar cells: mechanisms and physiological sequelae.American journal of physiology. Lung cellular and molecular physiology · 2017Review
- The pulmonary inflammatory response to multiwalled carbon nanotubes is influenced by gender and glutathione synthesis.Redox biology · 2016Article
- CFTR: A New Horizon in the Pathomechanism and Treatment of Pancreatitis.Reviews of physiology, biochemistry and pharmacology · 2016Review
- Cystic fibrosis transmembrane conductance regulator modulators in cystic fibrosis: current perspectives.Clinical pharmacology : advances and applications · 2016Review
- Antiinflammatory and Antimicrobial Effects of Thiocyanate in a Cystic Fibrosis Mouse Model.American journal of respiratory cell and molecular biology · 2015Article
- Influenza virus M2 targets cystic fibrosis transmembrane conductance regulator for lysosomal degradation during viral infection.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015Article
- Purification of the cystic fibrosis transmembrane conductance regulator protein expressed in Saccharomyces cerevisiae.Journal of visualized experiments : JoVE · 2014Article
- Polymorphisms in the glutathione pathway modulate cystic fibrosis severity: a cross-sectional study.BMC medical genetics · 2014Article
- Molecular identification and cellular localisation of GSH synthesis, uptake, efflux and degradation pathways in the rat ciliary body.Histochemistry and cell biology · 2013Article
- Glutathione efflux and cell death.Antioxidants & redox signaling · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
One of the most abundant antioxidants in the lung is glutathione (GSH), a low-molecular-weight thiol, which functions to attenuate both oxidative stress and inflammation. GSH is concentrated in the epithelial lining fluid (ELF) of the lung and can be elevated in response to the increased oxidant burden from cigarette smoke (CS). However, the transporter(s) responsible for the increase in ELF GSH with cigarette smoke is not known. Three candidate apical GSH transporters in the lung are CFTR, BCRP, and MRP2, but their potential roles in ELF GSH transport in response to CS have not been investigated. In vitro, the inhibition of CFTR, BCRP, or MRP2 resulted in decreased GSH efflux in response to cigarette smoke extract. In vivo, mice deficient in CFTR, BCRP, or MRP2 were exposed to either air or acute CS. CFTR-deficient mice had reduced basal and CS-induced GSH in the ELF, whereas BCRP or MRP2 deficiency had no effect on ELF GSH basal or CS-exposed levels. Furthermore, BCRP or MRP2 deficiency had little effect on lung tissue GSH. These data indicate that CFTR is predominantly involved in maintaining basal ELF GSH and increasing ELF GSH in response to CS.
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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.