Evidence map›Paper›PMID 19740254›Full record

ReviewRespirology (Carlton, Vic.)2009

Determinants of initiation and progression of idiopathic pulmonary fibrosis.

Robert Matthew Kottmann, Christopher M Hogan, Richard P Phipps, Patricia J Sime

Open access · bronzeAbstract readReview
In one paragraph

Review in Respirology (Carlton, Vic.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
6.5field-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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. IPF pathogenesis is dependent upon TGFβ induction of IGF-1.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Pharmacologic inhibition of lactate production prevents myofibroblast differentiation.American journal of physiology. Lung cellular and molecular physiology · 2015
    Article
  16. Article
  17. Fibrocytes in pulmonary fibrosis: a brief synopsis.European respiratory review : an official journal of the European Respiratory Society · 2013
    Review
  18. Article
  19. Article
  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

4 authors at 1 institution in 1 country.

Robert Matthew KottmannUniversity of Rochester School of Medicine, Rochester, NY 14642, USA.
Christopher M Hogan
Richard P Phipps
Patricia J Sime
University of Rochester · US

Funding

VISUAL INDICES OF NEUROTOXICITYP30ES001247 · NIEHS · UNIVERSITY OF ROCHESTER · PI Sally W Thurston · 1985 to 2026
$42.8M
Training in Environment ToxicologyT32ES007026 · NIEHS · UNIVERSITY OF ROCHESTER · PI Alison Elder, Marissa Sobolewski Terry · 1985 to 2026
$20.2M
MULTIDISCIPLINARY TRAINING IN PULMONARY RESEARCHT32HL066988 · NHLBI · UNIVERSITY OF ROCHESTER · PI GEORAS, STEVE N, O'REILLY, MICHAEL A · 2001 to 2021
$8.1M
Modulation of Silica-Induced Pulmonary FibrosisR01HL075432 · NHLBI · UNIVERSITY OF ROCHESTER · PI SIME, PATRICIA JANET · 2005 to 2009
$2.0M
Role of the Aryl Hydrocarbon Receptor in Lung InflammationR01HL088325 · NHLBI · UNIVERSITY OF ROCHESTER · PI SIME, PATRICIA JANET · 2008 to 2012
$1.9M
Pathways to FibrosisR03HL095402 · NHLBI · UNIVERSITY OF ROCHESTER · PI PHIPPS, RICHARD P., SIME, PATRICIA JANET · 2008 to 2009
$154k
NHLBI NIH HHS HL088325NHLBI NIH HHS HL095402NHLBI NIH HHS HL75432NHLBI NIH HHS R01 HL075432NHLBI NIH HHS R01 HL088325NHLBI NIH HHS R03 HL095402NHLBI NIH HHS T32 HL066988NHLBI NIH HHS T32 HL66988NIEHS NIH HHS ES 01247NIEHS NIH HHS P30 ES001247NIEHS NIH HHS T32 ES007026NIEHS NIH HHS T32 ES07026
6 · The paper itself

Abstract

IPF is a devastating disease with few therapeutic options. The precise aetiology of IPF remains elusive. However, our understanding of the pathologic processes involved in the initiation and progression of this disease is improving. Data on the mechanisms underlying IPF have been generated from epidemiologic investigations as well as cellular and molecular studies of human tissues. Although no perfect animal model of human IPF exists, pre-clinical animal studies have helped define pathways which are likely important in human disease. Epithelial injury, fibroblast activation and repetitive cycles of injury and abnormal repair are almost certainly key events. Factors which have been associated with initiation and/or progression of IPF include viral infections, abnormal cytokine, chemokine and growth factor production, oxidant stress, autoimmunity, inhalational of toxicants and gastro-oesophageal reflux disease. Furthermore, recent evidence identifies a role for a variety of genetic and epigenetic abnormalities ranging from mutations in surfactant protein C to abnormalities in telomere length and telomerase activity. The challenge remains to identify additional inciting agents and key dysregulated pathways that lead to disease progression so that we can develop targeted therapies to treat or prevent this serious disease.

Indexed as

Disease ProgressionAutoimmunityCytokinesHumansIdiopathic Pulmonary FibrosisMutationPulmonary Surfactant-Associated Protein CVirus DiseasesCytokinesPulmonary Surfactant-Associated Protein CSFTPC protein, human

Identifiers

PMID19740254
PMCPMC3884519
OpenAlexW1967913950

What OpenQuestion holds

Textmetadata
LicenceTDM
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.