Evidence map›Paper›PMID 29367207›Full record

ReviewGut2018

Non-alcoholic steatohepatitis pathogenesis: sublethal hepatocyte injury as a driver of liver inflammation.

Samar H Ibrahim, Petra Hirsova, Gregory J Gores

Abstract readReview
In one paragraph

Review in Gut, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 158 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
158citing papers in PubMed, 1 pooled it
21.9field-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

158 citing papers in PubMed, 1 synthesis or guideline pooled it, 259 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
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  6. Temporal Metabolomics Profiling Reveals Liver Metabolic Control in Single and Repeated Exhaustive Exercise in Murine Models.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  7. Article
  8. Article
  9. The neurobiological regulatory mechanism of brain edema.Frontiers in cellular neuroscience · 2026
    Review
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  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
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  20. Review

98 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

3 authors at 3 institutions in 2 countries.

Samar H IbrahimDivision of Pediatrics Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota, USA.
Petra HirsovaInstitute of Clinical Biochemistry and Diagnostics, University Hospital Hradec Kralove, Hradec Kralove, Czech Republic.
Gregory J GoresDivision of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota, USA.
Mayo Clinic · USUniversity Hospital Hradec Králové · CZWinnMed · US

Funding

MECHANISMS OF LIVER CELL INJURYR01DK041876 · NIDDK · MAYO CLINIC ROCHESTER · PI GORES, GREGORY J. · 1992 to 2019
$3.6M
MECHANISMS OF LIVER CELL INJURYR37DK041876 · NIDDK · MAYO CLINIC ROCHESTER · PI GORES, GREGORY J. · 2000 to 2009
$2.9M
Mentored Clinical Scientist Research Career Development (K08) research grantK08DK111397 · NIDDK · MAYO CLINIC ROCHESTER · PI IBRAHIM, SAMAR · 2017 to 2019
$498k
NIDDK NIH HHS K08 DK111397NIDDK NIH HHS R01 DK041876NIDDK NIH HHS R37 DK041876
6 · The paper itself

Abstract

A subset of patients with non-alcoholic fatty liver disease develop an inflammatory condition, termed non-alcoholic steatohepatitis (NASH). NASH is characterised by hepatocellular injury, innate immune cell-mediated inflammation and progressive liver fibrosis. The mechanisms whereby hepatic inflammation occurs in NASH remain incompletely understood, but appear to be linked to the proinflammatory microenvironment created by toxic lipid-induced hepatocyte injury, termed lipotoxicity. In this review, we discuss the signalling pathways induced by sublethal hepatocyte lipid overload that contribute to the pathogenesis of NASH. Furthermore, we will review the role of proinflammatory, proangiogenic and profibrotic hepatocyte-derived extracellular vesicles as disease biomarkers and pathogenic mediators during lipotoxicity. We also review the potential therapeutic strategies to block the feed-forward loop between sublethal hepatocyte injury and liver inflammation.

Indexed as

AnimalsHepatitisHepatocytesHumansLipidsLiverNon-alcoholic Fatty Liver DiseaseSignal TransductionLipidsinflammationnonalcoholic steatohepatitis

Identifiers

PMID29367207
PMCPMC5889737
OpenAlexW2784619339

What Socratic 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 Socratic graph.