Assessment of CFTR Dysfunction and Responsiveness to CFTR Modulators in COPD Bronchial Air-Liquid Interface Cultures.

Nikhil T Awatade, Kurtis F Budden, Prabuddha S Pathinayake, Andrew T Reid, Kristy S Nichol, Peter A B Wark

Abstract read

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Article in International journal of molecular sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed

–field-weighted citation impact

1 · What the graph read from it

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.

2 · The registry

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3 · Its place in the literature

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0 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Nikhil T AwatadeImmune Health Program, Hunter Medical Research Institute, School of Medicine and Public Health, University of Newcastle, Newcastle, NSW 2308, Australia.

Kurtis F BuddenImpact and Evaluation, Hunter Medical Research Institute, Locked Bag 1000, New Lambton Heights, Newcastle, NSW 2305, Australia.ORCID 0000-0002-7435-275X

Prabuddha S PathinayakeSchool of Medicine and Public Health, University of Newcastle, Newcastle, NSW 2308, Australia.ORCID 0000-0002-4947-5918

Andrew T ReidSchool of Medicine and Public Health, University of Newcastle, Newcastle, NSW 2308, Australia.

Kristy S NicholImmune Health Program, Hunter Medical Research Institute, School of Medicine and Public Health, University of Newcastle, Newcastle, NSW 2308, Australia.

Peter A B WarkImmune Health Program, Hunter Medical Research Institute, School of Medicine and Public Health, University of Newcastle, Newcastle, NSW 2308, Australia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increasing evidence suggests that acquired dysfunction of the cystic fibrosis transmembrane conductance regulator (CFTR) anion channel occurs as a result of cigarette smoke exposure in chronic obstructive pulmonary disease (COPD). CFTR-targeted therapies were developed to treat genetic CFTR defects in cystic fibrosis, but they have not demonstrated consistent clinical efficacy in small trials of patients with COPD. Here, we aimed to characterize CFTR and other ion channel activity and ciliation in primary bronchial epithelial cells (pBECs) from COPD donors compared with healthy controls, and to determine the extent to which CFTR dysfunction can be rescued by clinically relevant CFTR modulators. Air-liquid interface (ALI) cultures generated from conditionally reprogrammed (CR) primary bronchial epithelial cells (pBECs) obtained from healthy controls (

Indexed as

BronchiCystic Fibrosis Transmembrane Conductance RegulatorPulmonary Disease, Chronic ObstructiveAminophenolsCells, CulturedCiliaEpithelial CellsFemaleHumansMaleMiddle AgedQuinolonesAminophenolsCFTR protein, humanCystic Fibrosis Transmembrane Conductance RegulatorivacaftorQuinolonesair–liquid interfaceairway epitheliumCFTRCOPDicenticaftorivacaftor

Identifiers

PMID42884046

DOI10.3390/ijms27198803

PMCPMC13664796

What OpenQuestion holds

Textmetadata

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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.