Evidence map›Paper›PMID 23855302›Full record

ReviewJournal of gastroenterology and hepatology2013

Differences in innate immune signaling between alcoholic and non-alcoholic steatohepatitis.

Jan Petrasek, Timea Csak, Michal Ganz, Gyongyi Szabo

Abstract readReview
In one paragraph

Review in Journal of gastroenterology and hepatology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
–field-weighted citation impact
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

19 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Pattern Recognition Receptors: Significance of Expression in the Liver.Archivum immunologiae et therapiae experimentalis · 2020
    Review
  8. Review
  9. Review
  10. Differences in Posttransplant Hepatocellular Carcinoma Recurrence by Etiology of Liver Disease.Liver transplantation : official publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society · 2019
    Article
  11. Review
  12. New insights into Nod-like receptors (NLRs) in liver diseases.International journal of physiology, pathophysiology and pharmacology · 2018
    Review
  13. Review
  14. Review
  15. Inflammasome activation and function in liver disease.Nature reviews. Gastroenterology & hepatology · 2015
    Review
  16. Review
  17. Article
  18. Immune dysfunction in cirrhosis.World journal of gastroenterology · 2014
    Review
  19. 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

4 authors.

Jan PetrasekDepartment of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA.
Timea Csak
Michal Ganz
Gyongyi Szabo

Funding

PILOT AND FEASIBILITY PROGRAMP30DK032520 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI CZECH, MICHAEL P · 1986 to 2010
$14.6M
TLR4 Signaling in alcoholic liver diseaseR01AA017729 · NIAAA · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI SZABO, GYONGYI · 2009 to 2021
$4.3M
Toll like receptor - Mediated pathways in liver injuryR01DK075635 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI SZABO, GYONGYI · 2008 to 2011
$1.4M
Mechanisms of alcohol mediated organ and tissue damageR13AA017357 · NIAAA · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI SZABO, GYONGYI · 2008 to 2011
$112k
Mechanisms of Alcohol Mediated Organ and Tissue DamageR13AA015283 · NIAAA · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI SZABO, GYONGYI · 2004 to 2005
$40k
NIAAA NIH HHS AA017729NIAAA NIH HHS R01 AA017729NIAAA NIH HHS R13 AA015283NIAAA NIH HHS R13 AA017357NIDDK NIH HHS DK075635NIDDK NIH HHS DK32520NIDDK NIH HHS P30 DK032520NIDDK NIH HHS R01 DK075635
6 · The paper itself

Abstract

The similar histopathological characteristics of alcoholic steatohepatitis (ASH) and non-alcoholic steatohepatitis (NASH), and the crucial role of the innate immune response in both conditions may lead to the assumption that ASH and NASH represent the same pathophysiological entities caused by different risk factors. In this review paper, we elaborate on the pathophysiological differences between these two entities and highlight the disease-specific involvement of signaling molecules downstream of the Toll-like receptor 4, and the differential mechanism by which the inflammasome contributes to ASH versus NASH. Our findings emphasize that ASH and NASH have disease-specific mechanisms and therefore represent distinct biological entities. Further studies are needed to dissect the emerging differences in pathogenesis of these two conditions.

Indexed as

BacteriaFatty LiverFatty Liver, AlcoholicHumansImmunity, InnateInflammasomesInterleukin-1IntestinesLipopolysaccharidesNon-alcoholic Fatty Liver DiseaseRisk FactorsSignal TransductionToll-Like Receptor 4InflammasomesInterleukin-1LipopolysaccharidesToll-Like Receptor 4alcoholic liver diseasealcoholic steatohepatitisinflammasomeinnate immunityinterleukin-1 betainterleukin-1 receptor antagonistKupffer cellsnon-alcoholic steatohepatitisToll-like receptors

Identifiers

PMID23855302
PMCPMC3721424

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Registered trials

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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.