Evidence map›Paper›PMID 31380156›Full record

ArticleCurrent hepatology reports2018

Pathogenesis of NASH: The Impact of Multiple Pathways.

Mazen Noureddin, Arun J Sanyal

Abstract read
In one paragraph

Article in Current hepatology reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 1 pooled it
6.6field-weighted citation impact, top 3% 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

61 citing papers in PubMed, 1 synthesis or guideline pooled it, 125 citations in OpenAlex.

  1. Pooled it
  2. Multi-target protective effects ofPharmaceutical biology · 2026
    Article
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  4. Article
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  6. Review
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  11. Therapeutic Strategies for MASH: An Update on Drug Candidates Under Investigation in Late-Phase Clinical Trials.International journal of translational medicine (Basel, Switzerland) · 2025
    Article
  12. Review
  13. Review
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  15. Article
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  19. Article
  20. A study on the treatment effects ofFrontiers in veterinary science · 2024
    Article

1 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

2 authors at 2 institutions in 1 country.

Mazen NoureddinDirector, Fatty Liver Program and Associate Professor of Clinical Medicine, Division of Digestive and Liver Diseases, Comprehensive Transplant Program, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Arun J SanyalProfessor of Medicine, Physiology and Molecular Pathology, Division of Gastroenterology, Department of Internal Medicine, Virginia Commonwealth University School of Medicine, Richmond, Virginia, USA.
Cedars-Sinai Medical Center · USVirginia Commonwealth University · US

Funding

Training Grant in Digestive Diseases and Liver DiseasesT32DK007150 · NIDDK · VIRGINIA COMMONWEALTH UNIVERSITY · PI SANYAL, ARUN J · 1986 to 2017
$4.2M
LIPIDOMICS BASED DIAGNOSTICS FOR NONALCOHOLIC STEATOHEPATITISR01DK105961 · NIDDK · VIRGINIA COMMONWEALTH UNIVERSITY · PI DENNIS, EDWARD A, SANYAL, ARUN J · 2015 to 2018
$2.8M
NIDDK NIH HHS R01 DK105961NIDDK NIH HHS T32 DK007150
6 · The paper itself

Abstract

purpose of reviewAdvancing our understanding of the mechanisms that underlie NASH pathogenesis. RECENT

findingsRecent findings on NASH pathogenesis have expanded our understanding of its complexity including: (1) there are multiple parallel hits that lead to NASH; (2) the microbiota play an important role in pathogenesis, with bacterial species recently shown to accurately differentiate between NAFL and NASH patients; (3) the main drivers of liver cell injury are lipotoxicity caused by free fatty acids (FFAs) and their derivatives combined with mitochondrial dysfunction; (4) decreased endoplasmic reticulum (ER) efficiency with increased demand for protein synthesis/folding/repair results in ER stress, protracted unfolded protein response, and apoptosis; (5) upregulated proteins involved in multiple pathways including JNK, CHOP, PERK, BH3-only proteins, and caspases result in mitochondrial dysfunction and apoptosis; and (6) subtypes of NASH in which these pathophysiological pathways vary may require patient subtype identification to choose effective therapy. SUMMARY: Recent pathogenesis studies may lead to important therapeutic advances, already seen in patients treated with ACC, ASK1 and SCD1 inhibitors and FXR agonists. Further advancing our understanding of mechanisms underlying NASH pathogenesis and the complex interplay between them will be crucial for developing effective therapies.

Indexed as

cirrhosisfibrosismicrobiomeNonalcoholic fatty liver disease (NAFLD)Nonalcoholic steatohepatitis (NASH)ROS (reactive oxygen species)

Identifiers

PMID31380156
PMCPMC6677539
OpenAlexW2898705711

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.