Evidence map›Paper›PMID 30431350›Full record

ReviewAnnals of the American Thoracic Society2018

Mucociliary Defense: Emerging Cellular, Molecular, and Animal Models.

Kambez H Benam, Eszter K Vladar, William J Janssen, Christopher M Evans

Abstract readReview
In one paragraph

Review in Annals of the American Thoracic Society, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

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

17 citing papers in PubMed.

  1. Trial
  2. Review
  3. Review
  4. Article
  5. Emerging cell and molecular targets for treating mucus hypersecretion in asthma.Allergology international : official journal of the Japanese Society of Allergology · 2024
    Review
  6. Review
  7. Frontiers in immunology · 2024
    Review
  8. Alveolar epithelial regeneration in the aging lung.The Journal of clinical investigation · 2023
    Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Chair's Summary: Secreted Mucins in Lung Diseases.Annals of the American Thoracic Society · 2018
    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

4 authors.

Kambez H Benam1 Department of Medicine, Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Denver School of Medicine, Aurora, Colorado.ORCID 0000-0001-9117-3959
Eszter K Vladar1 Department of Medicine, Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Denver School of Medicine, Aurora, Colorado.ORCID 0000-0002-4160-8894
William J Janssen1 Department of Medicine, Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Denver School of Medicine, Aurora, Colorado.ORCID 0000-0002-6397-3454
Christopher M Evans1 Department of Medicine, Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Denver School of Medicine, Aurora, Colorado.ORCID 0000-0001-5600-7314

Funding

Tissue Bank and Biomarkers CoreP50CA058187 · NCI · UNIVERSITY OF COLORADO DENVER · PI MILLER, YORK E · 1992 to 2018
$43.8M
Role of Mucin in Lung Homeostasis and PathophysiologyR01HL080396 · NHLBI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Christopher M Evans · 2009 to 2026
$8.6M
Lung Macrophage Programming in Acute Lung InjuryR35HL140039 · NHLBI · NATIONAL JEWISH HEALTH · PI JANSSEN, WILLIAM · 2018 to 2024
$6.4M
Mechanisms of lung macrophage programming by MUC5B during health and diseaseR01HL130938 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI EVANS, CHRISTOPHER M · 2016 to 2025
$5.2M
NCI NIH HHS P50 CA058187NHLBI NIH HHS R01 HL080396NHLBI NIH HHS R01 HL130938NHLBI NIH HHS R35 HL140039
6 · The paper itself

Abstract

Respiratory tissues are bombarded by billions of particles daily. If allowed to accumulate, these particles can cause injury, inflammation, or infection, and thus may significantly disrupt airflow and gas exchange. Mucociliary defense, a primary mechanism for protecting host tissues, operates through the coordinated functions of mucus and cilia that trap and eliminate inhaled materials. Mucociliary function is also required for the elimination of endogenous cells and debris. Although defense is necessarily robust, it is also tightly regulated to minimize physiologic disruption of the host. Indeed, mucociliary dysfunction contributes to the pathogenesis of many lung diseases-including asthma, chronic obstructive pulmonary disease, pulmonary fibrosis, and cystic fibrosis-in which airflow limitation, inflammation, persistent tissue injury, and structural remodeling occur. Here, we highlight recent advances in cilia and mucin biology, the importance of well-controlled mucociliary interactions, and the need to better understand how these regulate innate barrier and immune defense.

Indexed as

AnimalsCiliaDisease Models, AnimalHumansLung DiseasesMucinsMucociliary ClearanceMucinsairway epitheliumgoblet cellmucinmucus

Identifiers

PMID30431350
PMCPMC6322027

What OpenQuestion holds

Textmetadata
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.