Evidence map›Paper›PMID 36108172›Full record

ArticleAmerican journal of respiratory cell and molecular biology2022

Anomalous Epithelial Variations and Ectopic Inflammatory Response in Chronic Obstructive Pulmonary Disease.

Naoaki Watanabe, Yu Fujita, Jun Nakayama, Yutaro Mori, Tsukasa Kadota, Yusuke Hayashi, Iwao Shimomura, Takashi Ohtsuka, Koji Okamoto, Jun Araya and 2 more

Abstract read
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In one paragraph

Article in American journal of respiratory cell and molecular biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 2 pooled it
13.3field-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

53 citing papers in PubMed, 2 syntheses or guidelines pooled it, 66 citations in OpenAlex.

  1. Pooled it
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  11. Hallmarks of the ageing lung: 10 years later.The European respiratory journal · 2026
    Review
  12. TGFb signaling instructs a conserved fibrosis-associated cell state marked by LRRC15.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
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  19. Cellular plasticity and regenerative mechanisms in the lung.European respiratory review : an official journal of the European Respiratory Society · 2026
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 2 institutions in 2 countries.

Naoaki WatanabeLaboratory of Integrative Oncology and.
Yu FujitaDivision of Respiratory Diseases, Department of Internal Medicine, and.ORCID 0000-0002-8916-7303
Jun NakayamaLaboratory of Integrative Oncology and.
Yutaro MoriDivision of Cancer Differentiation, National Cancer Center Research Institute, Tokyo, Japan.
Tsukasa KadotaDivision of Respiratory Diseases, Department of Internal Medicine, and.ORCID 0000-0002-9533-7241
Yusuke HayashiLaboratory of Integrative Oncology and.
Iwao ShimomuraLaboratory of Integrative Oncology and.
Takashi OhtsukaDivision of Thoracic Surgery, Department of Surgery, The Jikei University School of Medicine, Tokyo, Japan.
Koji OkamotoDivision of Cancer Differentiation, National Cancer Center Research Institute, Tokyo, Japan.
Jun ArayaDivision of Respiratory Diseases, Department of Internal Medicine, and.
Kazuyoshi KuwanoDivision of Respiratory Diseases, Department of Internal Medicine, and.
Yusuke YamamotoLaboratory of Integrative Oncology and.
Jikei University School of Medicine · JPLaboratoire d’immunologie intégrative du cancer · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Phenotypic alterations in the lung epithelium have been widely implicated in chronic obstructive pulmonary disease (COPD) pathogenesis, but the precise mechanisms orchestrating this persistent inflammatory process remain unknown because of the complexity of lung parenchymal and mesenchymal architecture. To identify cell type-specific mechanisms and cell-cell interactions among the multiple lung resident cell types and inflammatory cells that contribute to COPD progression, we profiled 57,918 cells from lungs of patients with COPD, smokers without COPD, and never-smokers using single-cell RNA sequencing technology. We predicted pseudotime of cell differentiation and cell-to-cell interaction networks in COPD. Although epithelial components in never-smokers were relatively uniform, smoker groups represent extensive heterogeneity in epithelial cells, particularly in alveolar type 2 (AT2) clusters. Among AT2 cells, which are generally regarded as alveolar progenitors, we identified a unique subset that increased in patients with COPD and specifically expressed a series of chemokines including CXCL1 and CXCL8. A trajectory analysis revealed that the inflammatory AT2 cell subpopulation followed a unique differentiation path, and a prediction model of cell-to-cell interactions inferred significantly increased intercellular networks of inflammatory AT2 cells. Our results identify previously unidentified cell subsets and provide an insight into the biological and clinical characteristics of COPD pathogenesis.

Indexed as

Pulmonary Disease, Chronic ObstructiveAlveolar Epithelial CellsCell DifferentiationEpithelial CellsHumansLungalveolar type 2 cellcell-to-cell interactionchronic obstructive pulmonary diseasesingle-cell RNA sequencing

Identifiers

PMID36108172
OpenAlexW4295932348

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.