Evidence map›Paper›PMID 28878132›Full record

ReviewJCI insight2017

Therapeutic opportunities for alcoholic steatohepatitis and nonalcoholic steatohepatitis: exploiting similarities and differences in pathogenesis.

Thomas Greuter, Harmeet Malhi, Gregory J Gores, Vijay H Shah

Abstract readReview
In one paragraph

Review in JCI insight, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
–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

37 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. MetALD: Clinical aspects, pathophysiology and treatment.JHEP reports : innovation in hepatology · 2025
    Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Epigenetics of alcohol-related liver diseases.JHEP reports : innovation in hepatology · 2022
    Review
  16. Article
  17. Article
  18. Review
  19. The knowns and unknowns of treatment for alcoholic hepatitis.The lancet. Gastroenterology & hepatology · 2020
    Review
  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

4 authors.

Thomas GreuterDivision of Gastroenterology and Hepatology, University Hospital Zurich, Zurich, Switzerland.
Harmeet MalhiGastroenterology Research Unit, Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota, USA.
Gregory J GoresGastroenterology Research Unit, Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota, USA.
Vijay H ShahGastroenterology Research Unit, Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota, USA.

Funding

TREAT-MayoU01AA021788 · NIAAA · MAYO CLINIC ROCHESTER · PI MALHI, HARMEET, SHAH, VIJAY H. · 2012 to 2022
$4.7M
Pathobiology of Liver InjuryR01DK111378 · NIDDK · MAYO CLINIC ROCHESTER · PI MALHI, HARMEET · 2016 to 2025
$3.9M
MECHANISMS OF LIVER CELL INJURYR01DK041876 · NIDDK · MAYO CLINIC ROCHESTER · PI GORES, GREGORY J. · 1992 to 2019
$3.6M
Molecular Mechanisms of Liver Fibrosis (Diversity Supplement)R37AA021171 · NIAAA · MAYO CLINIC ROCHESTER · PI VIJAY H. SHAH · 2019 to 2026
$3.0M
MECHANISMS OF LIVER CELL INJURYR37DK041876 · NIDDK · MAYO CLINIC ROCHESTER · PI GORES, GREGORY J. · 2000 to 2009
$2.9M
Molecular Mechanisms of Liver FibrosisR01AA021171 · NIAAA · MAYO CLINIC ROCHESTER · PI SHAH, VIJAY H. · 2012 to 2018
$2.5M
Organelle Dysfunction in Liver InflammationR03DK107402 · NIDDK · MAYO CLINIC ROCHESTER · PI MALHI, HARMEET · 2016 to 2017
$159k
NIAAA NIH HHS R01 AA021171NIAAA NIH HHS R37 AA021171NIAAA NIH HHS U01 AA021788NIDDK NIH HHS R01 DK041876NIDDK NIH HHS R01 DK111378NIDDK NIH HHS R03 DK107402NIDDK NIH HHS R37 DK041876
6 · The paper itself

Abstract

Alcoholic steatohepatitis (ASH) and nonalcoholic steatohepatitis (NASH) are among the most frequent causes of chronic liver disease in the United States. Although the two entities are triggered by different etiologies - chronic alcohol consumption (ASH) and obesity-associated lipotoxicity (NASH) - they share overlapping histological and clinical features owing to common pathogenic mechanisms. These pathogenic processes include altered hepatocyte lipid metabolism, organelle dysfunction (i.e., ER stress), hepatocyte apoptosis, innate immune system activation, and hepatic stellate cell activation. Nonetheless, there are several disease-specific molecular signaling pathways, such as differential pathway activation downstream of TLR4 (MyD88-dependence in NASH versus MyD88-independence in ASH), inflammasome activation and IL-1β signaling in ASH, insulin resistance and lipotoxicity in NASH, and dysregulation of different microRNAs, which clearly highlight that ASH and NASH are two distinct biological entities. Both pathogenic similarities and differences have therapeutic implications. In this Review, we discuss these pathogenic mechanisms and their therapeutic implications for each disease, focusing on both shared and distinct targets.

Indexed as

Fatty Liver, AlcoholicHumansNon-alcoholic Fatty Liver DiseaseApoptosis pathwaysCell stressHepatitisHepatologyTherapeutics

Identifiers

PMID28878132
PMCPMC5621906

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.