Evidence map›Paper›PMID 10931794›Full record

ReviewEnvironmental health perspectives2000

Interstitial fibrosis and growth factors.

J A Lasky, A R Brody

Open access · diamondAbstract readReview
In one paragraph

Review in Environmental health perspectives, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
7.7field-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

43 citing papers in PubMed, 127 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Plumbagin attenuates Bleomycin-induced lung fibrosis in mice.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2022
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Gastric Acid and Pepsin Work Together in Simulated Gastric Acid Inhalation Leading to Pulmonary Fibrosis in Rats.Medical science monitor : international medical journal of experimental and clinical research · 2019
    Article
  12. Article
  13. Article
  14. Article
  15. Myofibroblast repair mechanisms post-inflammatory response: a fibrotic perspective.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2017
    Review
  16. Article
  17. Article
  18. Expression of WNT5A in Idiopathic Pulmonary Fibrosis and Its Control by TGF-β and WNT7B in Human Lung Fibroblasts.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2016
    Article
  19. Role of caveolae in high glucose and TGF-β₁ induced fibronectin production in rat mesangial cells.International journal of clinical and experimental pathology · 2014
    Article
  20. 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

2 authors at 1 institution in 1 country.

J A LaskySection of Pulmonary Diseases, Critical Care and Environmental Medicine, Department of Medicine, and the Lung Biology Program, Tulane University Medical Center, New Orleans, Louisiana, USA.
A R Brody
Tulane Medical Center · US

Funding

TNF-alpha to TGF-beta Signal TransductionR01ES006766 · NIEHS · TULANE UNIVERSITY OF LOUISIANA · PI BRODY, ARNOLD RALPH · 1994 to 2008
$2.4M
TGF-B in Interstitial Lung DiseaseR01HL060532 · NHLBI · TULANE UNIVERSITY OF LOUISIANA · PI BRODY, ARNOLD RALPH · 1997 to 2005
$1.9M
AUTOCRINE PDGF DEPENDENT FIBROBLAST PROLIFERATIONK08HL003374 · NHLBI · TULANE UNIVERSITY OF LOUISIANA · PI LASKY, JOSEPH A · 1995 to 1998
–
NHLBI NIH HHS K08 HL 03374NHLBI NIH HHS R0 1HL60532NIEHS NIH HHS R01 ES06766
6 · The paper itself

Abstract

Interstitial pulmonary fibrosis (IPF) is scarring of the lung caused by a variety of inhaled agents including mineral particles, organic dusts, and oxidant gases. The disease afflicts millions of individuals worldwide, and there are no effective therapeutic approaches. A major reason for this lack of useful treatments is that few of the molecular mechanisms of disease have been defined sufficiently to design appropriate targets for therapy. Our laboratory has focused on the molecular mechanisms through which three selected peptide growth factors could play a role in the development of IPF. Hundreds of growth factors and cytokines could be involved in the complex disease process. We are studying platelet-derived growth factor because it is the most potent mesenchymal cell mitogen yet described, transforming growth factor beta because it is a powerful inducer of extracellular matrix (scar tissue) components by mesenchymal cells, and tumor necrosis factor alpha because it is a pleiotropic cytokine that we and others have shown is essential for the development of IPF in animal models. This review describes some of the evidence from studies in humans, in animal models, and in vitro, that supports the growth factor hypothesis. The use of modern molecular and transgenic technologies could elucidate those targets that will allow effective therapeutic approaches.

Indexed as

Air PollutantsAnimalsGrowth SubstancesHumansInhalation ExposureLung Diseases, InterstitialPulmonary FibrosisAir PollutantsGrowth Substances

Identifiers

PMID10931794
PMCPMC1637668
OpenAlexW2128743400

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.