Evidence map›Paper›PMID 38073611›Full record

ArticleInternational forum of allergy & rhinology2024

Hypoxia-induced cystic fibrosis transmembrane conductance regulator dysfunction is a universal mechanism underlying reduced mucociliary transport in sinusitis.

Do-Yeon Cho, Shaoyan Zhang, T Graham Norwood, Daniel Skinner, Tonja A Hollis, Marie L Ehrhardt, Lydia C Yang, Dong-Jin Lim, Jessica W Grayson, Ahmed Lazrak and 3 more

Open access · greenAbstract read
In one paragraph

Article in International forum of allergy & rhinology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.0field-weighted citation impact, top 20% of its field
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

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.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Lipopolysaccharide Causes Acquired CFTR Dysfunction in Murine Nasal Airways.Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery · 2025
    Article
  5. Acquired dysfunction of CFTR underlies cystic fibrosis-like disease of the canine gallbladder.American journal of physiology. Gastrointestinal and liver physiology · 2024
    Article
  6. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 1 institution in 1 country.

Do-Yeon ChoDepartment of Otolaryngology-Head & Neck Surgery, University of Alabama at Birmingham, Birmingham, Alabama, USA.ORCID 0000-0002-5173-8959
Shaoyan ZhangDepartment of Otolaryngology-Head & Neck Surgery, University of Alabama at Birmingham, Birmingham, Alabama, USA.
T Graham NorwoodDepartment of Otolaryngology-Head & Neck Surgery, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Daniel SkinnerDepartment of Otolaryngology-Head & Neck Surgery, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Tonja A HollisDepartment of Otolaryngology-Head & Neck Surgery, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Marie L EhrhardtDepartment of Otolaryngology-Head & Neck Surgery, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Lydia C YangDepartment of Otolaryngology-Head & Neck Surgery, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Dong-Jin LimDepartment of Otolaryngology-Head & Neck Surgery, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Jessica W GraysonDepartment of Otolaryngology-Head & Neck Surgery, University of Alabama at Birmingham, Birmingham, Alabama, USA.ORCID 0000-0002-2131-8005
Ahmed LazrakGregory Fleming James Cystic Fibrosis Research Center, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Sadis MatalonGregory Fleming James Cystic Fibrosis Research Center, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Steven M RoweGregory Fleming James Cystic Fibrosis Research Center, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Bradford A WoodworthDepartment of Otolaryngology-Head & Neck Surgery, University of Alabama at Birmingham, Birmingham, Alabama, USA.ORCID 0000-0003-3292-9167
University of Alabama at Birmingham · US

Funding

UAB CF Research and Translation Core CenterP30DK072482 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI AMIT GAGGAR · 2007 to 2026
$23.0M
Bromine Inhalation Induced Lung Injury: Novel Mechanisms and Treatment StrategiesU01ES026458 · NIEHS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MATALON, SADIS · 2015 to 2019
$3.9M
CIALIS® reverses halogen induced injury to pregnant animals and their offspringU01ES027697 · NIEHS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI JILLING, TAMAS SANDOR, MATALON, SADIS · 2016 to 2020
$3.7M
Ivacaftor for Acquired CFTR Dysfunction in Chronic RhinosinusitisR01HL133006 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI WOODWORTH, BRADFORD ALAN · 2016 to 2020
$1.7M
Chloride secretagogues for acquired CFTR dysfunction in chronic rhinosinusitisK08HL107142 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI WOODWORTH, BRADFORD ALAN · 2011 to 2015
$668k
Dysbiosis of the Sinus Microbiota in Chronic RhinosinusitisK08AI146220 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CHO, DO-YEON · 2019 to 2021
$467k
Impact of mucin fermenting microbes on the virulence of Pseudomonas aeruginosa in chronic rhinosinusitisR21AI168894 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CHO, DO-YEON · 2022 to 2023
$408k
A Ginsenoside TMEM16A Potentiator for Cystic FibrosisR21AT012234 · NCCIH · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI WOODWORTH, BRADFORD ALAN · 2023 to 2024
$405k
Cystic Fibrosis Foundation 002481G221National Institute of Allergy and Infectious Diseases K08AI146220-03NCCIH NIH HHS R21 AT012234NCCIH NIH HHS R21AT012234-01NHLBI NIH HHS HL107142-05NHLBI NIH HHS K08 HL107142NHLBI NIH HHS R01 HL133006NHLBI NIH HHS R01 HL133006-05NIAID NIH HHS K08 AI146220NIAID NIH HHS R21 AI168894NIDDK NIH HHS 5P30DK072482-05NIDDK NIH HHS P30 DK072482NIEHS NIH HHS 3UO1 ES026458 03S1NIEHS NIH HHS 5UO1 ES026458NIEHS NIH HHS 5UO1 ES027697NIEHS NIH HHS U01 ES026458NIEHS NIH HHS U01 ES027697
6 · The paper itself

Abstract

introductionHypoxia due to sinus obstruction is a major pathogenic mechanism leading to sinusitis. The objective of the current study is to define the electrophysiologic characteristics of hypoxia in vitro and in vivo.

methodsCystic fibrosis bronchoepithelial cells expressing wild-type cystic fibrosis transmembrane conductance regulator (CFTR) and human sinonasal epithelial cells were exposed to 1% or atmospheric O

resultsUssing chamber (p < 0.05), whole-cell (p < 0.001), and single channel patch-clamp (p < 0.0001) showed significant inhibition of Cl

conclusionHypoxia induces severe CFTR dysfunction via free radical production causing reduced MCT in vitro and in vivo. Improved oxygenation is critical to reducing the impact of persistent mucociliary dysfunction.

Indexed as

Cystic Fibrosis Transmembrane Conductance RegulatorHypoxiaMucociliary ClearanceSinusitisAnimalsCystic FibrosisEpithelial CellsFree RadicalsHumansHypoxia-Inducible Factor 1, alpha SubunitNasal MucosaRabbitsCFTR protein, humanCystic Fibrosis Transmembrane Conductance RegulatorFree RadicalsHypoxia-Inducible Factor 1, alpha Subunitairway surface liquidCFTRchronic rhinosinusitischronic sinusitisfunctional microanatomyglutathionehypoxiamucociliary transportoptical coherence tomographypatch clamppericiliary liquidpotential differencerabbit sinusitissinusitis

Identifiers

PMID38073611
PMCPMC11849962
OpenAlexW4389571562

What OpenQuestion holds

Textmetadata
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Read underepoch 390

Registered trials

None linked

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.