Evidence map›Paper›PMID 8550840›Full record

ArticleThe Journal of clinical investigation1996

Bleomycin-induced pulmonary fibrosis in transgenic mice that either lack or overexpress the murine plasminogen activator inhibitor-1 gene.

D T Eitzman, R D McCoy, X Zheng, W P Fay, T Shen, D Ginsburg, R H Simon

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 182 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
182citing papers in PubMed, 1 pooled it
29.7field-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

182 citing papers in PubMed, 1 synthesis or guideline pooled it, 559 citations in OpenAlex.

  1. Guideline
  2. Trial
  3. Blood transcriptomic signatures distinguishEmerging microbes & infections · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Frontiers in pharmacology · 2025
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. PTPα promotes fibroproliferative responses after acute lung injury.American journal of physiology. Lung cellular and molecular physiology · 2022
    Article
  19. Article
  20. Article

122 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

7 authors at 3 institutions in 2 countries.

D T EitzmanDivision of Cardiology, University of Michigan Medical Center, Ann Arbor 48109, USA.
R D McCoy
X Zheng
W P Fay
T Shen
D Ginsburg
R H Simon
Howard Hughes Medical Institute · USPulmonary and Critical Care Associates · USUniversity of Michigan–Ann Arbor · US

Funding

PEPTIDE INHIBITION OF PLASMINOGEN ACTIVATOR INHIBITOR 1F32HL009104 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI EITZMAN, DANIEL T · 1994 to 1995
–
STRUCTURE/FUNCTION IN PLASMINOGEN ACTIVATOR INHIBITOR-1K08HL002728 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI FAY, WILLIAM P · 1992 to 1996
–
HUMAN PLASMINOGEN ACTIVATOR-INHIBITOR PAI-1 GENER01HL039137 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI GINSBURG, DAVID · 1987 to 1991
–
NHLBI NIH HHS HL-02728NHLBI NIH HHS HL-09104NHLBI NIH HHS HL-39137
6 · The paper itself

Abstract

Impaired fibrinolytic activity within the lung is a common manifestation of acute and chronic inflammatory lung diseases. Because the fibrinolytic system is active during repair processes that restore injured tissues to normal, reduced fibrinolytic activity may contribute to the subsequent development of pulmonary fibrosis. To examine the relationship between the fibrinolytic system and pulmonary fibrosis, lung inflammation was induced by bleomycin in transgenic mice that either overexpressed or were completely deficient in murine plasminogen activator inhibitor-1 (PAI-1). 2 wk after 0.075 U of bleomycin, the lungs of transgenic mice overexpressing PAI-1 contained significantly more hydroxyproline (118 +/- 8 micrograms) than littermate controls (70.5 +/- 8 micrograms, P < 0.005). 3 wk after administration of a higher dose of bleomycin (0.15 U), the lung hydroxyproline content of mice completely deficient in PAI-1 (49 +/- 8 micrograms) was not significantly different (P = 0.63) than that of control animals receiving saline (37 +/- 1 micrograms), while hydroxyproline content was significantly increased in heterozygote (77 +/- 12 micrograms, P = 0.06) and wild-type (124 +/- 19 micrograms, P < 0.001) littermates. These data demonstrate a direct correlation between the genetically determined level of PAI-1 expression and the extent of collagen accumulation that follows inflammatory lung injury. These results strongly support the hypothesis that alterations in fibrinolytic activity influence the extent of pulmonary fibrosis that occurs after inflammatory injury.

Indexed as

AnimalsBleomycinFemaleFibrinolysisHydroxyprolineLungMaleMiceMice, KnockoutMice, TransgenicPlasminogen Activator Inhibitor 1Pulmonary FibrosisBleomycinHydroxyprolinePlasminogen Activator Inhibitor 1

Identifiers

PMID8550840
PMCPMC507084
OpenAlexW2044478331

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.