Evidence map›Paper›PMID 32941426›Full record

ArticlePloS one2020

Dysregulation of club cell biology in idiopathic pulmonary fibrosis.

Wu-Lin Zuo, Mahboubeh R Rostami, Michelle LeBlanc, Robert J Kaner, Sarah L O'Beirne, Jason G Mezey, Philip L Leopold, Karsten Quast, Sudha Visvanathan, Jay S Fine and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.0field-weighted citation impact, top 7% 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

32 citing papers in PubMed, 46 citations in OpenAlex.

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  11. From Epithelium to Therapy: Transitional Cells in Lung Fibrosis.American journal of respiratory cell and molecular biology · 2025
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Cell-cell interactions and communication dynamics in lung fibrosis.Chinese medical journal pulmonary and critical care medicine · 2024
    Review
  18. Review
  19. Review
  20. 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

12 authors at 3 institutions in 2 countries.

Wu-Lin ZuoDepartment of Genetic Medicine, Weill Cornell Medical College, New York, New York, United States of America.
Mahboubeh R RostamiDepartment of Genetic Medicine, Weill Cornell Medical College, New York, New York, United States of America.
Michelle LeBlancDepartment of Genetic Medicine, Weill Cornell Medical College, New York, New York, United States of America.
Robert J KanerDepartment of Genetic Medicine, Weill Cornell Medical College, New York, New York, United States of America.
Sarah L O'BeirneDepartment of Genetic Medicine, Weill Cornell Medical College, New York, New York, United States of America.
Jason G MezeyDepartment of Genetic Medicine, Weill Cornell Medical College, New York, New York, United States of America.
Philip L LeopoldDepartment of Genetic Medicine, Weill Cornell Medical College, New York, New York, United States of America.
Karsten QuastBoehringer Ingelheim Pharma GmbH & Co. KG, Biberach an der Riss, Germany.
Sudha VisvanathanBoehringer Ingelheim Pharmaceuticals, Ridgefield, Connecticut, United States of America.
Jay S FineBoehringer Ingelheim Pharmaceuticals, Ridgefield, Connecticut, United States of America.
Matthew J ThomasBoehringer Ingelheim Pharma GmbH & Co. KG, Biberach an der Riss, Germany.
Ronald G CrystalDepartment of Genetic Medicine, Weill Cornell Medical College, New York, New York, United States of America.ORCID 0000-0001-6177-6839
Cornell University · USBoehringer Ingelheim (Germany) · DEBoehringer Ingelheim (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a progressive, chronic fibrotic lung disease with an irreversible decline of lung function. "Bronchiolization", characterized by ectopic appearance of airway epithelial cells in the alveolar regions, is one of the characteristic features in the IPF lung. Based on the knowledge that club cells are the major epithelial secretory cells in human small airways, and their major secretory product uteroglobin (SCGB1A1) is significantly increased in both serum and epithelial lining fluid of IPF lung, we hypothesize that human airway club cells contribute to the pathogenesis of IPF. By assessing the transcriptomes of the single cells from human lung of control donors and IPF patients, we identified two SCGB1A1+ club cell subpopulations, highly expressing MUC5B, a significant genetic risk factor strongly associated with IPF, and SCGB3A2, a marker heterogeneously expressed in the club cells, respectively. Interestingly, the cellular proportion of SCGB1A1+MUC5B+ club cells was significantly increased in IPF patients, and this club cell subpopulation highly expressed genes related to mucous production and immune cell chemotaxis. In contrast, though the cellular proportion did not change, the molecular phenotype of the SCGB1A1+SCGB3A2high club cell subpopulation was significantly altered in IPF lung, with increased expression of mucins, cytokine and extracellular matrix genes. The single cell transcriptomic analysis reveals the cellular and molecular heterogeneity of club cells, and provide novel insights into the biological functions of club cells in the pathogenesis of IPF.

Indexed as

TranscriptomeBronchiolesHumansIdiopathic Pulmonary FibrosisLungRespiratory MucosaSecretoglobinsSingle-Cell AnalysisUteroglobinSCGB1A1 protein, humanSCGB3A2 protein, humanSecretoglobinsUteroglobin

Identifiers

PMID32941426
PMCPMC7498242
OpenAlexW3087159033

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.