ReviewProceedings of the American Thoracic Society2010
Role of endoplasmic reticulum stress in cystic fibrosis-related airway inflammatory responses.
Review in Proceedings of the American Thoracic Society, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
48 citing papers in PubMed, 77 citations in OpenAlex.
- Prevalent gut phages encode modular adhesins mediating epithelial binding and endoplasmic reticulum trafficking.Nature communications · 2026Article
- VPS26A retromer complex and SNX27 mediate stress-induced Golgi bypass of membrane proteins.Nature communications · 2026Article
- Host transcriptomic analysis reveals a defective intracellular environment that limits SARS-CoV-2 replication in CFTR-deficient airway epithelium.Frontiers in cellular and infection microbiology · 2026Article
- CFTR Modulators Counteract F508del CFTR Functional Defects in a Pancreatic Epithelial Model of Cystic Fibrosis.Life (Basel, Switzerland) · 2025Article
- Redox Imbalance in Cystic Fibrosis: The Multifaceted Role of Oxidative Stress.Pharmaceuticals (Basel, Switzerland) · 2025Review
- p.Phe508del-CFTR Trafficking: A Protein Quality Control Perspective Through UPR, UPS, and Autophagy.International journal of molecular sciences · 2025Review
- 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
- Autophagy in the lung: guardian of homeostasis or driver of disease.Autophagy reports · 2025Review
- The F508del-CFTR trafficking correctors elexacaftor and tezacaftor are CFTR-independent CaRespiratory research · 2024Article
- Combined exercise training decreases blood pressure in OLDER women withEpigenetics · 2024Article
- Article
- Understanding the impact of ER stress on lung physiology.Frontiers in cell and developmental biology · 2024Review
- ERdj5 protects goblet cells from endoplasmic reticulum stress-mediated apoptosis under inflammatory conditions.Experimental & molecular medicine · 2023Article
- Cystic fibrosis rabbits develop spontaneous hepatobiliary lesions and CF-associated liver disease (CFLD)-like phenotypes.PNAS nexus · 2023Article
- The Impact of Highly Effective Modulator Therapy on Cystic Fibrosis Microbiology and Inflammation.Clinics in chest medicine · 2022Review
- A Splice Switch in SIGIRR Causes a Defect of IL-37-Dependent Anti-Inflammatory Activity in Cystic Fibrosis Airway Epithelial Cells.International journal of molecular sciences · 2022Article
- Culture with apically applied healthy or disease sputum alters the airway surface liquid proteome and ion transport across human bronchial epithelial cells.American journal of physiology. Cell physiology · 2021Article
- The Interplay between the Unfolded Protein Response, Inflammation and Infection in Cystic Fibrosis.Cells · 2021Review
- Copper-Associated Oxidative Stress Contributes to Cellular Inflammatory Responses in Cystic Fibrosis.Biomedicines · 2021Article
- IRE1α Is a Therapeutic Target for Cystic Fibrosis Airway Inflammation.International journal of molecular sciences · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Chronic airway infection and inflammation are hallmarks of cystic fibrosis (CF) pulmonary disease. The altered airway environment resulting from infection and inflammation can affect the innate defense of the airway epithelia. Luminal bacterial and inflammatory stimuli trigger an adaptation in human airway epithelia, characterized by a hyperinflammatory response to inflammatory mediators, which is mediated by an expansion of the endoplasmic reticulum (ER) and its Ca(2+) stores. Recent studies demonstrated that a form of ER stress, the unfolded protein response (UPR), is activated in airway epithelia by bacterial infection-induced airway inflammation. UPR-dependent signaling is responsible for the ER Ca(2+) store expansion-mediated amplification of airway inflammatory responses. These studies highlight the functional importance of the UPR in airway inflammation and suggest that targeting the UPR may be a therapeutic strategy for airway diseases typified by chronic inflammation. This article reviews the contribution of airway epithelia to airway inflammatory responses, discusses how expansion of the ER Ca(2+) stores in inflamed airway epithelia contributes to airway inflammation, describes the functional role of the UPR in these processes, and discusses how UPR activation might be relevant for CF airways inflammatory disease.
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What Socratic holds
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 Socratic graph.