Evidence map›Paper›PMID 21501583›Full record

ArticleArchives of biochemistry and biophysics2011

Plasminogen activator inhibitor-1 deficient mice are protected from angiotensin II-induced fibrosis.

Juliane I Beier, J Phillip Kaiser, Luping Guo, Manuel Martínez-Maldonado, Gavin E Arteel

Abstract read
In one paragraph

Article in Archives of biochemistry and biophysics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 22% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Alcoholic liver disease: Utility of animal models.World journal of gastroenterology · 2018
    Review
  7. Article
  8. Article
  9. Article
  10. Kupffer cells in the liver.Comprehensive Physiology · 2013
    Review
  11. Article
  12. Article
  13. 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

5 authors at 1 institution in 1 country.

Juliane I BeierDepartment of Pharmacology and Toxicology, University of Louisville Health Sciences Center, KY 40292, USA. juliane.beier@louisville.edu
J Phillip Kaiser
Luping Guo
Manuel Martínez-Maldonado
Gavin E Arteel
University of Louisville · US

Funding

UOFL ENVIRONMENTAL HEALTH SCIENCES TRAINING PROGRAMT32ES011564 · NIEHS · UNIVERSITY OF LOUISVILLE · PI David W Hein, John Pierce Wise · 2004 to 2026
$7.1M
CONTROL OF DRUG AND ETHANOL METABOLISMR01AA003624 · NIAAA · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI ARTEEL, GAVIN E · 1985 to 2010
$2.3M
CONTROL OF DRUG AND ETHANOL METABOLISMR37AA003624 · NIAAA · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI THURMAN, RONALD G · 1999 to 2000
$280k
The role of PKC epsilon in alcoholic liver diseaseF31AA017346 · NIAAA · UNIVERSITY OF LOUISVILLE · PI KAISER, JONATHAN PHILLIP · 2007 to 2010
$71k
NIAAA NIH HHS AA003624NIAAA NIH HHS F31 AA017346NIAAA NIH HHS R01 AA003624NIAAA NIH HHS R37 AA003624NIEHS NIH HHS T32 ES011564
6 · The paper itself

Abstract

PAI-1 has been shown to be both profibrotic and antifibrotic in animal models of hepatic fibrosis. Although these models have similarities to human fibrotic liver disease, no rodent model completely recapitulates the clinical situation; indeed, transaminase values in most models of hepatic fibrosis are much higher than in chronic liver diseases in humans. Here, wild-type and PAI-1(-/-) mice were administered AngII (500 ng/kg/min) for 4 weeks. ECM accumulation was evaluated by Sirius red staining, hydroxyproline content, and fibrin and collagen immunostaining. Induction of pro-fibrotic genes was assessed by real-time RT-PCR. Despite the absence of any significant liver damage, AngII infusion increased the deposition of hepatic collagen and fibrin ECM, with a perisinusoidal pattern. PAI-1(-/-) mice were protected from these ECM changes, indicating a causal role of PAI-1 in this fibrosis model. Protection in the knockout strain correlated with a blunted increase in αSMA, and elevated activities of matrix metalloproteinases (MMP2, MMP9). These data suggest that PAI-1 plays a critical role in mediating fibrosis caused by AngII and lends weight-of-evidence to a pro-fibrotic role of this protein in liver. Furthermore, the current study proposes a new model of 'pure' hepatic fibrosis in mice with little inflammation or hepatocyte death.

Indexed as

Angiotensin IIAnimalsCollagenExtracellular MatrixGene DeletionHumansLiverLiver CirrhosisMaleMiceMice, Inbred C57BLMice, KnockoutPlasminogen Activator Inhibitor 1Angiotensin IICollagenPlasminogen Activator Inhibitor 1

Identifiers

PMID21501583
PMCPMC3095665
OpenAlexW2001471898

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.