Evidence map›Paper›PMID 30833143›Full record

ReviewRedox biology2019

Redox regulation of motile cilia in airway disease.

Michael E Price, Joseph H Sisson

Open access · goldAbstract readReview
In one paragraph

Review in Redox biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 9% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.

  1. A molecular systems architecture of asthma.Frontiers in immunology · 2026
    Pooled it
  2. Article
  3. Primary cilia dysfunction: A critical driver of metabolic diseases (Review).International journal of molecular medicine · 2026
    Review
  4. Review
  5. The alcohol exposome.Alcohol (Fayetteville, N.Y.) · 2025
    Review
  6. Review
  7. Ciliary Function, Antigen Stasis and Asthma.International journal of molecular sciences · 2024
    Review
  8. Article
  9. Antigen stasis and airway nitrosative stress in human primary ciliary dyskinesia.American journal of physiology. Lung cellular and molecular physiology · 2024
    Article
  10. Mitochondrial uncoupling proteins protect human airway epithelial ciliated cells from oxidative damage.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  11. Article
  12. Review
  13. Mucociliary clearance augmenting drugs block SARS-CoV-2 replication in human airway epithelial cells.American journal of physiology. Lung cellular and molecular physiology · 2023
    Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Review
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

2 authors at 1 institution in 1 country.

Michael E PriceUniversity of Nebraska Medical Center, Pulmonary, Critical Care, Sleep & Allergy Division, Department of Internal Medicine, Omaha, NE, USA; University of Nebraska Medical Center, Department of Cellular & Integrative Physiology, Omaha, NE, USA. Electronic address: michael.price@unmc.edu.
Joseph H SissonUniversity of Nebraska Medical Center, Pulmonary, Critical Care, Sleep & Allergy Division, Department of Internal Medicine, Omaha, NE, USA. Electronic address: jsisson@unmc.edu.
University of Nebraska Medical Center · US

Funding

Alcohol drives S-nitrosylation to impair airway mucociliary clearanceF30AA024676 · NIAAA · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI PRICE, MICHAEL E · 2015 to 2019
$191k
NIAAA NIH HHS F30 AA024676
6 · The paper itself

Abstract

Motile cilia on airway cells are necessary for clearance of mucus-trapped particles out of the lung. Ciliated airway epithelial cells are uniquely exposed to oxidants through trapping of particles, debris and pathogens in mucus and the direct exposure to inhaled oxidant gases. Dynein ATPases, the motors driving ciliary motility, are sensitive to the local redox environment within each cilium. Several redox-sensitive cilia-localized proteins modulate dynein activity and include Protein Kinase A, Protein Kinase C, and Protein Phosphatase 1. Moreover, cilia are rich in known redox regulatory proteins and thioredoxin domain-containing proteins that are critical in maintaining a balanced redox environment. Importantly, a nonsense mutation in TXNDC3, which contains a thioredoxin motif, has recently been identified as disease-causing in Primary Ciliary Dyskinesia, a hereditary motile cilia disease resulting in impaired mucociliary clearance. Here we review current understanding of the role(s) oxidant species play in modifying airway ciliary function. We focus on oxidants generated in the airways, cilia redox targets that modulate ciliary beating and imbalances in redox state that impact health and disease. Finally, we review disease models such as smoking, asthma, alcohol drinking, and infections as well as the direct application of oxidants that implicate redox balance as a modulator of cilia motility.

Indexed as

AnimalsCiliaCyclic AMP-Dependent Protein KinasesHumansOxidantsOxidation-ReductionProtein Kinase CProtein Phosphatase 1Respiratory Tract DiseasesThioredoxinsCyclic AMP-Dependent Protein KinasesOxidantsProtein Kinase CProtein Phosphatase 1ThioredoxinsAlcoholCiliaHydrogen peroxideNitric oxideRedox regulationS-nitrosationSuperoxide

Identifiers

PMID30833143
PMCPMC6859573
OpenAlexW2916217735

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.