Evidence map›Paper›PMID 19129758›Full record

ReviewMucosal immunology2009

Pulmonary fibrosis: pathogenesis, etiology and regulation.

M S Wilson, T A Wynn

Open access · bronzeAbstract readReview
In one paragraph

Review in Mucosal immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 445 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
445citing papers in PubMed, 4 pooled it
29.9field-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

445 citing papers in PubMed, 4 syntheses or guidelines pooled it, 815 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Trial
  6. Article
  7. Early and matureBiofilm · 2026
    Article
  8. Article
  9. Article
  10. Association ofInternational journal of molecular sciences · 2026
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Olfactory immunity: defending the neural-mucosal barrier.Journal of immunology (Baltimore, Md. : 1950) · 2026
    Review
  18. Article
  19. Article
  20. Review

385 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

2 authors at 1 institution in 1 country.

M S WilsonImmunopathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA. wilsonmar@niaid.nih.gov
T A Wynn
National Institutes of Health · US

Funding

Approaches To Immunological Intervention In SchistosomiasisZIAAI000829 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI WYNN, THOMAS · 2009 to 2018
$9.9M
Mechanisms of Fibrosis in Asthma and Other Fibroproliferative DiseasesZIAAI001019 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI WYNN, THOMAS · 2009 to 2018
$7.1M
Mechanisms of Fibrosis in Asthma and Other Fibroproliferative DiseasesZ01AI001019 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI WYNN, THOMAS · 2007 to 2008
$635k
Intramural NIH HHS Z01 AI001019
6 · The paper itself

Abstract

Pulmonary fibrosis and architectural remodeling of tissues can severely disrupt lung function, often with fatal consequences. The etiology of pulmonary fibrotic diseases is varied, with an array of triggers including allergens, chemicals, radiation and environmental particles. However, the cause of one of the most common pulmonary fibrotic conditions, idiopathic pulmonary fibrosis (IPF), is still unclear. This review examines common mechanisms of pulmonary wound-healing responses following lung injury, and highlights the pathogenesis of some of the most widespread pulmonary fibrotic diseases. A three phase model of wound repair is reviewed that includes; (1) injury; (2) inflammation; and (3) repair. In most pulmonary fibrotic conditions dysregulation at one or more of these phases has been reported. Chronic inflammation can lead to an imbalance in the production of chemokines, cytokines, growth factors, and disrupt cellular recruitment. These changes coupled with excessive pro-fibrotic IL-13 and/or TGFbeta1 production can turn a well-controlled healing response into a pathogenic fibrotic response. Endogenous regulatory mechanisms are discussed including novel areas of therapeutic intervention. Restoring homeostasis to these dysregulated healing responses, or simply neutralizing the key pro-fibrotic mediators may prevent or slow the progression of pulmonary fibrosis.

Indexed as

AnimalsAsthmaCollagenCytokinesFibroblastsHumansHypersensitivityIdiopathic Pulmonary FibrosisIntercellular Signaling Peptides and ProteinsInterleukin-13Lung InjuryPulmonary FibrosisRegenerationTransforming Growth Factor beta1CollagenCytokinesIntercellular Signaling Peptides and ProteinsInterleukin-13Transforming Growth Factor beta1

Identifiers

PMID19129758
PMCPMC2675823
OpenAlexW2064307892

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.