Evidence map›Paper›PMID 33968032›Full record

ArticleFrontiers in immunology2021

The NLRP3-Inflammasome-Caspase-1 Pathway Is Upregulated in Idiopathic Pulmonary Fibrosis and Acute Exacerbations and Is Inducible by Apoptotic A549 Cells.

Benedikt Jäger, Benjamin Seeliger, Oliver Terwolbeck, Gregor Warnecke, Tobias Welte, Meike Müller, Christian Bode, Antje Prasse

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
5.9field-weighted citation impact, top 3% 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

  1. Pooled it
  2. Acute exacerbation in fibrotic interstitial lung disease: an international working group report.American journal of respiratory and critical care medicine · 2026
    Review
  3. Review
  4. Altered cholesterol immunometabolism activates the macrophage NLRP3-inflammasome in lung fibrosis.American journal of respiratory cell and molecular biology · 2026
    Article
  5. Defective efferocytosis in diabetes: molecular mechanisms and emerging therapeutic strategies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  6. Review
  7. Article
  8. Article
  9. Altered Metabolism in Idiopathic Pulmonary Fibrosis.Journal of cellular physiology · 2025
    Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Journal of biomedical research · 2024
    Article
  17. Article
  18. Regulation of alveolar macrophage death in pulmonary fibrosis: a review.Apoptosis : an international journal on programmed cell death · 2023
    Review
  19. PANoptosis: Mechanism and Role in Pulmonary Diseases.International journal of molecular sciences · 2023
    Review
  20. Role of mitochondrial stress and the NLRP3 inflammasome in lung diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    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

8 authors at 5 institutions in 1 country.

Benedikt JägerFraunhofer Institute for Toxicology and Experimental Medicine, Hannover, Germany.
Benjamin SeeligerDepartment of Respiratory Medicine, Hannover Medical School and Biomedical Research in End-stage and Obstructive Lung Disease (BREATH), German Center for Lung Research (DZL), Hannover, Germany.
Oliver TerwolbeckFraunhofer Institute for Toxicology and Experimental Medicine, Hannover, Germany.
Gregor WarneckeDepartment of Heart, Thoracic, Transplantation and Vascular Surgery, Hannover Medical School, Hannover, Germany.
Tobias WelteDepartment of Respiratory Medicine, Hannover Medical School and Biomedical Research in End-stage and Obstructive Lung Disease (BREATH), German Center for Lung Research (DZL), Hannover, Germany.
Meike MüllerFraunhofer Institute for Toxicology and Experimental Medicine, Hannover, Germany.
Christian BodeDepartment of Anesthesiology and Intensive Care Medicine, University Hospital Bonn, Bonn, Germany.
Antje PrasseFraunhofer Institute for Toxicology and Experimental Medicine, Hannover, Germany.
Fraunhofer Institute for Toxicology and Experimental Medicine · DEGerman Center for Lung Research · DEMedizinische Hochschule Hannover · DEUniversity Hospital Bonn · DEUniversity of Freiburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a relentlessly progressive disease harboring significant morbidity and mortality despite recent advances in therapy. Regardless of disease severity acute exacerbations (IPF-AEs) may occur leading to considerable loss of function and are the leading cause of death in IPF. Histologic features of IPF-AE are very similar to acute respiratory distress syndrome (ARDS), but the underlying mechanisms are incompletely understood. We investigated the role of the NLRP3 inflammasome in IPF and IPF-AE. Bronchoalveolar lavage (BAL) cells were sampled from patients with IPF (n = 32), IPF-AE (n = 10), ARDS (n = 7) and healthy volunteers (HV, n = 37) and the NLRP3-inflammasome was stimulated

Indexed as

ApoptosisA549 CellsAcute DiseaseAdultAgedAged, 80 and overCaspase 1Cathepsin BFemaleHumansIdiopathic Pulmonary FibrosisInflammasomesInterleukin-1MaleMiddle AgedNLR Family, Pyrin Domain-Containing 3 ProteinCaspase 1Cathepsin BInflammasomesInterleukin-1interleukin 1 precursorNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanProtein PrecursorsReactive Oxygen Speciesacute exacerbationidiopathic pulmonary fibrosisinflammasomeinflammationNLRP3

Identifiers

PMID33968032
PMCPMC8104027
OpenAlexW3157538149

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.