Evidence map›Paper›PMID 22238286›Full record

ReviewExperimental biology and medicine (Maywood, N.J.)2012

Alcoholic liver disease and the potential role of plasminogen activator inhibitor-1 and fibrin metabolism.

Juliane I Beier, Gavin E Arteel

Open access · greenAbstract readReview
In one paragraph

Review in Experimental biology and medicine (Maywood, N.J.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 2 pooled it
3.5field-weighted citation impact, top 7% 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

34 citing papers in PubMed, 2 syntheses or guidelines pooled it, 60 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Review
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  13. Review
  14. Article
  15. Exploring the Complex Role of Coagulation Factor VIII in Chronic Liver Disease.Cellular and molecular gastroenterology and hepatology · 2021
    Review
  16. The Matrisome, Inflammation, and Liver Disease.Seminars in liver disease · 2020
    Review
  17. Article
  18. Article
  19. Plasminogen Activator Inhibitor-1 Is Critical in Alcohol-Enhanced Acute Lung Injury in Mice.American journal of respiratory cell and molecular biology · 2017
    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

2 authors at 1 institution in 1 country.

Juliane I BeierDepartment of Pharmacology and Toxicology and University of Louisville Alcohol Research Center, University of Louisville Health Sciences Center, Louisville, KY 40292, USA.
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
NIAAA NIH HHS AA003624NIAAA NIH HHS R01 AA003624NIAAA NIH HHS R37 AA003624NIEHS NIH HHS T32 ES011564
6 · The paper itself

Abstract

Plasminogen activator inhibitor-1 (PAI-1) is a major player in fibrinolysis due to its classical role of inhibiting plasminogen activators. Although increased fibrinolysis is common in alcoholic cirrhosis, decreased fibrinolysis (driven mostly by elevated levels of PAI-1) is common during the development of alcoholic liver disease (ALD). However, whether or not PAI-1 plays a causal role in the development of early ALD was unclear. Recent studies in experimental models have suggested that PAI-1 may contribute to the development of early (steatosis), intermediate (steatohepatitis) and late (fibrosis) stages of ALD. For example, fatty liver owing to both acute and chronic ethanol was blunted by the genetic inhibition of PAI-1. This effect of targeting PAI-1 appears to be mediated, at least in part, by an increase in very low-density lipoprotein (VLDL) synthesis in the genetic absence of this acute phase protein. Results from a two-hit model employing ethanol and lipopolysaccharide administration suggest that PAI-1 plays a critical role in hepatic inflammation, most likely due to its ability to cause fibrin accumulation, which subsequently sensitizes the liver to ensuing damaging insults. Lastly, the role of PAI-1 in hepatic fibrosis is less clear and appears that PAI-1 may serve a dual role in this pathological change, both protective (enhancing regeneration) and damaging (blocking matrix degradation). In summary, results from these studies suggest that PAI-1 may play multiple roles in the various stages of ALD, both protective and damaging. The latter effect is mediated by its influence on steatosis (i.e. decreasing VLDL synthesis), inflammation (i.e. impairing fibrinolysis) and fibrosis (i.e. blunting matrix degradation), whereas the former is mediated by maintaining hepatocyte division after an injury.

Indexed as

AnimalsDisease ProgressionEthanolFatty LiverFibrinFibrinolysisHumansLipopolysaccharidesLipoproteins, VLDLLiverLiver Cirrhosis, AlcoholicLiver Diseases, AlcoholicMicePlasminogen Activator Inhibitor 1EthanolFibrinLipopolysaccharidesLipoproteins, VLDLPlasminogen Activator Inhibitor 1SERPINE1 protein, human

Identifiers

PMID22238286
PMCPMC5047512
OpenAlexW2076295447

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.