ArticleThe Journal of biological chemistry2014
Cigarette smoke-induced Ca2+ release leads to cystic fibrosis transmembrane conductance regulator (CFTR) dysfunction.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
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Who cites it
68 citing papers in PubMed, 96 citations in OpenAlex.
- Patient-derived organoids reveal ductal dysfunction and CFTR-modulator responses in chronic pancreatitis.Cell stem cell · 2026Article
- Review
- Health effects of black and blond tobacco: a comparative analysis on smoking-related diseases with emphasis on bronchitis and COPD.Frontiers in public health · 2026Article
- Unraveling molecular mechanisms of cigarette smoke bitterness via chemical profiling and bitter taste receptor activation analysis.Scientific reports · 2025Article
- Therapeutic strategies to reverse cigarette smoke-induced ion channel and mucociliary dysfunction in COPD airway epithelial cells.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Secondhand vape exposure regulation of CFTR and immune function in cystic fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- CFTR as a therapeutic target for severe lung infection.American journal of physiology. Lung cellular and molecular physiology · 2025Review
- Association between biomarkers of tobacco smoke exposure and clinical efficacy of ivacaftor in the G551D observational trial (GOAL).Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2024Observational
- Vaping-Induced Proteolysis Causes Airway Surface Dehydration.International journal of molecular sciences · 2023Article
- Aiming to Improve Equity in Pulmonary Health: Cystic Fibrosis.Clinics in chest medicine · 2023Review
- 30-Min Exposure to Tobacco Smoke Influences Airway Ion Transport-An In Vitro Study.Current oncology (Toronto, Ont.) · 2023Article
- Furin as a therapeutic target in cystic fibrosis airways disease.European respiratory review : an official journal of the European Respiratory Society · 2023Review
- The COPD-Associated Polymorphism Impairs the CFTR Function to Suppress Excessive IL-8 Production upon Environmental Pathogen Exposure.International journal of molecular sciences · 2023Article
- Extracellular Vesicles' Role in the Pathophysiology and as Biomarkers in Cystic Fibrosis and COPD.International journal of molecular sciences · 2022Review
- The deleterious effects of smoking on the development and progression of chronic pancreatitis.Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] · 2022Review
- Socioeconomic determinants of respiratory health in patients with cystic fibrosis: implications for treatment strategies.Expert review of respiratory medicine · 2022Review
- Current clinical opinion on CFTR dysfunction and patient risk of pancreatitis: diagnostic and therapeutic considerations.Expert review of gastroenterology & hepatology · 2022Article
- Left behind: The potential impact of CFTR modulators on racial and ethnic disparities in cystic fibrosis.Paediatric respiratory reviews · 2022Review
- Endolysosomal Cation Channels and Lung Disease.Cells · 2022Review
- Review
8 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Chronic obstructive pulmonary disease affects 64 million people and is currently the fourth leading cause of death worldwide. Chronic obstructive pulmonary disease includes both emphysema and chronic bronchitis, and in the case of chronic bronchitis represents an inflammatory response of the airways that is associated with mucus hypersecretion and obstruction of small airways. Recently, it has emerged that exposure to cigarette smoke (CS) leads to an inhibition of the cystic fibrosis transmembrane conductance regulator (CFTR) Cl(-) channel, causing airway surface liquid dehydration, which may play a role in the development of chronic bronchitis. CS rapidly clears CFTR from the plasma membrane and causes it to be deposited into aggresome-like compartments. However, little is known about the mechanism(s) responsible for the internalization of CFTR following CS exposure. Our studies revealed that CS triggered a rise in cytoplasmic Ca(2+) that may have emanated from lysosomes. Furthermore, chelation of cytoplasmic Ca(2+), but not inhibition of protein kinases/phosphatases, prevented CS-induced CFTR internalization. The macrolide antibiotic bafilomycin A1 inhibited CS-induced Ca(2+) release and prevented CFTR clearance from the plasma membrane, further linking cytoplasmic Ca(2+) and CFTR internalization. We hypothesize that CS-induced Ca(2+) release prevents normal sorting/degradation of CFTR and causes internalized CFTR to reroute to aggresomes. Our data provide mechanistic insight into the potentially deleterious effects of CS on airway epithelia and outline a hitherto unrecognized signaling event triggered by CS that may affect the long term transition of the lung into a hyper-inflammatory/dehydrated environment.
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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.