Evidence map›Paper›PMID 33262481›Full record

ReviewExperimental & molecular medicine2020

Interleukin-11 signaling underlies fibrosis, parenchymal dysfunction, and chronic inflammation of the airway.

Benjamin Ng, Stuart A Cook, Sebastian Schafer

Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in Experimental & molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05536375 (A Pilot Feasibility Study of Detection of IL-11 and Other Cytokines in the Exhaled Breath Condensate), which is not on this map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
7.3field-weighted citation impact, top 2% 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.

NCT05536375 nacompletednot on this mapstarted 2022, after this paper: background citation

A Pilot Feasibility Study of Detection of IL-11 and Other Cytokines in the Exhaled Breath Condensate (EBC) and Blood of Healthy Volunteers

TypeinterventionalSponsorNational Heart Centre SingaporeRan2022 to 2023Enrolled25ConditionsHealthyArmsExhaled breath condensate collection and blood draw
3 · Its place in the literature

Who cites it

58 citing papers in PubMed, 103 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. The role of IL-11 in chronic diseases.Frontiers in immunology · 2026
    Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. 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

3 authors at 2 institutions in 2 countries.

Benjamin NgNational Heart Research Institute Singapore, National Heart Centre Singapore, Singapore, Singapore.ORCID http://orcid.org/0000-0001-8970-0932
Stuart A CookNational Heart Research Institute Singapore, National Heart Centre Singapore, Singapore, Singapore.
Sebastian SchaferNational Heart Research Institute Singapore, National Heart Centre Singapore, Singapore, Singapore. sebastian@duke-nus.edu.sg.
National University of Singapore · SGDuke-NUS Medical School · SG

Funding

Medical Research Council MC_U120085815MOH | National Medical Research Council (NMRC) NMRC/STaR/0011/2012MOH | National Medical Research Council (NMRC) NMRC/STaR/0029/2017MOH | National Medical Research Council (NMRC) OFYIRG18nov-0014
6 · The paper itself

Abstract

Interleukin (IL)-11 evolved as part of the innate immune response. In the human lung, IL-11 upregulation has been associated with viral infections and a range of fibroinflammatory diseases, including idiopathic pulmonary fibrosis. Transforming growth factor-beta (TGFβ) and other disease factors can initiate an autocrine loop of IL-11 signaling in pulmonary fibroblasts, which, in a largely ERK-dependent manner, triggers the translation of profibrotic proteins. Lung epithelial cells also express the IL-11 receptor and transition into a mesenchymal-like state in response to IL-11 exposure. In mice, therapeutic targeting of IL-11 with antibodies can arrest and reverse bleomycin-induced pulmonary fibrosis and inflammation. Intriguingly, fibroblast-specific blockade of IL-11 signaling has anti-inflammatory effects, which suggests that lung inflammation is sustained, in part, through IL-11 activity in the stroma. Proinflammatory fibroblasts and their interaction with the damaged epithelium may represent an important but overlooked driver of lung disease. Initially thought of as a protective cytokine, IL-11 is now increasingly recognized as an important determinant of lung fibrosis, inflammation, and epithelial dysfunction.

Indexed as

Signal TransductionAnimalsBiomarkersCellular SenescenceCytokinesDisease SusceptibilityFibroblastsFibrosisHumansInflammationInflammation MediatorsInterleukin-11MAP Kinase Signaling SystemRespiratory Function TestsRespiratory Tract DiseasesBiomarkersCytokinesInflammation MediatorsInterleukin-11

Identifiers

PMID33262481
PMCPMC7705429
OpenAlexW3107804499

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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.