Evidence map›Paper›PMID 20008134›Full record

ArticleThe American journal of pathology2010

Tissue factor-deficiency and protease activated receptor-1-deficiency reduce inflammation elicited by diet-induced steatohepatitis in mice.

James P Luyendyk, Bradley P Sullivan, Grace L Guo, Ruipeng Wang

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

31 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
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  7. Caspase Inhibition Reduces Hepatic Tissue Factor-Driven Coagulation In Vitro and In Vivo.Toxicological sciences : an official journal of the Society of Toxicology · 2018
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  16. Fas-induced apoptosis increases hepatocyte tissue factor procoagulant activity in vitro and in vivo.Toxicological sciences : an official journal of the Society of Toxicology · 2014
    Article
  17. Review
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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.

James P LuyendykDepartment of Pharmacology, Toxicology and Therapeutics, The University of Kansas Medical Center, 3901 Rainbow Blvd, MS-1018, Kansas City, KS 66160, USA. jluyendyk@kumc.edu
Bradley P Sullivan
Grace L Guo
Ruipeng Wang
University of Kansas Medical Center · US

Funding

THE ROLE OF HUMAN PXR IN ANTI-TUBERCULOSIS DRUG-INDUCED LIVER INJURYP20RR021940 · NCRR · UNIVERSITY OF KANSAS MEDICAL CENTER · PI KLASSEN, CURTIS D · 2006 to 2011
$12.1M
Tissue specific mechanism of FXR in suppressing bile-acid synthesisR01DK081343 · NIDDK · UNIVERSITY OF KANSAS MEDICAL CENTER · PI GUO, GRACE L · 2008 to 2011
$1.3M
NCRR NIH HHS P20 RR021940NIDDK NIH HHS R01 DK081343NIDDK NIH HHS R01DK081343
6 · The paper itself

Abstract

Altered hepatic lipid homeostasis, hepatocellular injury, and inflammation are features of nonalcoholic steatohepatitis, which contributes significantly to liver-related morbidity and mortality in the Western population. A collection of inflammatory mediators have been implicated in the pathogenesis of steatohepatitis in mouse models. However, the pathways essential for coordination and amplification of hepatic inflammation and injury caused by steatosis are not completely understood. We tested the hypothesis that tissue factor (TF)-dependent thrombin generation and the thrombin receptor protease activated receptor-1 (PAR-1) contribute to liver inflammation induced by steatosis in mice. Wild-type C57Bl/6J mice fed a diet deficient in methionine and choline for 2 weeks manifested steatohepatitis characterized by increased serum alanine aminotransferase activity, macrovesicular hepatic steatosis, hepatic inflammatory gene expression, and lobular inflammation. Steatohepatitis progression was associated with thrombin generation and hepatic fibrin deposition. Coagulation cascade activation was significantly reduced in low TF mice, which express 1% of normal TF levels. Hepatic triglyceride accumulation was not affected in low TF mice or PAR-1-deficient mice. In contrast, biomarkers of hepatocellular injury, inflammatory gene induction, and hepatic accumulation of macrophages and neutrophils were greatly reduced by TF-deficiency and PAR-1-deficiency. The results suggest that TF-dependent thrombin generation and activation of PAR-1 amplify hepatic inflammation and injury during the pathogenesis of steatohepatitis.

Indexed as

Alanine TransaminaseAnimalsBlood CoagulationBlood Coagulation FactorsChemokine CCL2CholineDietFatty LiverGene Expression RegulationInflammationLiverMethionineMiceMice, Inbred C57BLModels, BiologicalReceptor, PAR-1Alanine TransaminaseBlood Coagulation FactorsCcl2 protein, mouseChemokine CCL2CholineMethionineReceptor, PAR-1ThrombinThromboplastinTriglycerides

Identifiers

PMID20008134
PMCPMC2797880
OpenAlexW2155368247

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.