Evidence map›Paper›PMID 30431340›Full record

ReviewAnnals of the American Thoracic Society2018

Airway Epithelial Differentiation and Mucociliary Clearance.

Jeffrey A Whitsett

Open access · greenAbstract 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 206 papers.

0numbers the graph read from it
0cells of the map it votes in
206citing papers in PubMed
16.9field-weighted citation impact, top 1% 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

206 citing papers in PubMed, 305 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Structural and cellular mechanisms of mucus plugging in the larger airways.Chinese medical journal pulmonary and critical care medicine · 2026
    Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Airway Goblet Metaplasia Resulting from YAP/TAZ Deletion Drives Pulmonary Inflammatory Responses.American journal of respiratory cell and molecular biology · 2026
    Article

146 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

Jeffrey A WhitsettDivision of Pulmonary Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio.ORCID 0000-0003-1668-5174
Cincinnati Children's Hospital Medical Center · US

Funding

Transcriptional Programming of Asthma Related Pathology in Respiratory EpitheliaR01HL095580 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI WHITSETT, JEFFREY A · 2009 to 2017
$4.7M
"Lung MAP" Atlas Research CenterU01HL122642 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI POTTER, S. STEVEN, WHITSETT, JEFFREY A · 2014 to 2018
$3.9M
Airway Progenitor Cell Profileration and Differentiation During Lung RepairU01HL110964 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI STREETER, PHILIP R, WHITSETT, JEFFREY A · 2012 to 2016
$3.3M
NHLBI NIH HHS R01 HL095580NHLBI NIH HHS U01 HL110964NHLBI NIH HHS U01 HL122642
6 · The paper itself

Abstract

The lung is continuously exposed to particles, toxicants, and microbial pathogens that are cleared by a complex mechanical, innate, and acquired immune system. Mucociliary clearance, mediated by the actions of diverse conducting airway and submucosal gland epithelial cells, plays a critical role in a multilayered defense system by secreting fluids, electrolytes, antimicrobial and antiinflammatory proteins, and mucus onto airway surfaces. The mucociliary escalator removes particles and pathogens by the mechanical actions of cilia and cough. Abnormalities in mucociliary clearance, whether related to impaired fluid secretion, ciliary dysfunction, lack of cough, or the disruption of epithelial cells lining the respiratory tract, contribute to the pathogenesis of common chronic pulmonary disorders. Although mucus and other airway epithelial secretions play a critical role in protecting the lung during acute injury, impaired mucus clearance after chronic mucus hyperproduction causes airway obstruction and infection, which contribute to morbidity in common pulmonary disorders, including chronic obstructive pulmonary disease, asthma, idiopathic pulmonary fibrosis, cystic fibrosis, bronchiectasis, and primary ciliary dyskinesia. In this summary, the molecular and cellular mechanisms mediating airway mucociliary clearance, as well as the role of goblet cell metaplasia and mucus hyperproduction, in the pathogenesis of chronic respiratory diseases are considered.

Indexed as

Cell DifferentiationCiliaEpithelial CellsHumansLung DiseasesMucinsMucociliary ClearanceMucusMucinsairway ciliated cellsgoblet cellmucus hyperproduction

Identifiers

PMID30431340
PMCPMC6322033
OpenAlexW2900535696

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.