Evidence map›Paper›PMID 17961066›Full record

ReviewAntioxidants & redox signaling2008

The role of inflammation in the pathogenesis of idiopathic pulmonary fibrosis.

Benjamin D Bringardner, Christopher P Baran, Timothy D Eubank, Clay B Marsh

Abstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 156 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
156citing papers in PubMed, 4 pooled it
9.0field-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.

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

156 citing papers in PubMed, 4 syntheses or guidelines pooled it, 314 citations in OpenAlex.

  1. Pooled it
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  4. Pooled it
  5. Trial
  6. Article
  7. Article
  8. Review
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  12. Review
  13. Article
  14. Beyond classical collagen: basement membrane collagen IV in age-associated lung diseases.European respiratory review : an official journal of the European Respiratory Society · 2025
    Review
  15. Pulmonary fibrosis: from mechanisms to therapies.Journal of translational medicine · 2025
    Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

96 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

4 authors at 1 institution in 1 country.

Benjamin D BringardnerDepartment of Internal Medicine, Division of Pulmonary, Allergy, Critical Care, and Sleep Medicine, The Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio 43210, USA.
Christopher P Baran
Timothy D Eubank
Clay B Marsh
The Ohio State University · US

Funding

Myofibroblasts and fibrosis after cardiac transplantP01HL070294 · NHLBI · OHIO STATE UNIVERSITY · PI MARSH, CLAY B · 2001 to 2005
$6.3M
NF-kappaB:an Akt target &regulator of monocyte survivalR01HL067176 · NHLBI · OHIO STATE UNIVERSITY · PI MARSH, CLAY B · 2001 to 2011
$3.2M
Targeting myofibroblast activation in chronic fibrotic diseaseR01HL085109 · NHLBI · OHIO STATE UNIVERSITY · PI STRAUCH, ARTHUR ROGER · 2008 to 2011
$1.5M
A NEW PARADIGM FOR FIBROSIS: MONOCYTE ACTIVATION OF TGFR01HL066108 · NHLBI · OHIO STATE UNIVERSITY · PI MARSH, CLAY B · 2001 to 2004
$1.2M
The human correlation: studies of data obtained from a mouse model of IPFR03HL095431 · NHLBI · OHIO STATE UNIVERSITY · PI BARAN, CHRISTOPHER · 2008 to 2009
$150k
NHLBI NIH HHS 1R01HL085109NHLBI NIH HHS 2R01HL067176NHLBI NIH HHS 5R01HL066108-04NHLBI NIH HHS 5R01HL67176-04NHLBI NIH HHS P01 HL070294NHLBI NIH HHS P01HL70294NHLBI NIH HHS R01 HL066108NHLBI NIH HHS R01 HL067176NHLBI NIH HHS R01 HL085109NHLBI NIH HHS R03 HL095431
6 · The paper itself

Abstract

The role of inflammation in idiopathic pulmonary fibrosis (IPF) is controversial. If inflammation were critical to the disease process, lung pathology would demonstrate an influx of inflammatory cells, and that the disease would respond to immunosuppression. Neither is true. The classic pathology does not display substantial inflammation, and no modulation of the immune system is effective as treatment. Recent data suggest that the pathophysiology of the disease is more a product of fibroblast dysfunction than of dysregulated inflammation. The role of inflammation in disease pathogenesis comes from pathology from atypical patients, biologic samples procured during exacerbations of the disease, and careful examination of biologic specimens from patients with stable disease. We suggest that inflammation is indeed a critical factor in IPF and propose five potential nontraditional mechanisms for the role of inflammation in the pathogenesis of IPF: the direct inflammatory hypothesis, the matrix hypothesis, the growth factor-receptor hypothesis, the plasticity hypothesis, and the vascular hypothesis. To address these, we review the literature exploring the differences in pathology, prognosis, and clinical course, as well as the role of cytokines, growth factors, and other mediators of inflammation, and last, the role of matrix and vascular supply in patients with IPF.

Indexed as

AnimalsAsbestosDisease Models, AnimalHumansInflammationLung InjuryModels, BiologicalPulmonary CirculationPulmonary FibrosisSmokingAsbestos

Identifiers

PMID17961066
PMCPMC2737712
OpenAlexW2070054912

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.