Evidence map›Paper›PMID 33343375›Full record

ReviewFrontiers in pharmacology2020

Non-Alcoholic Steatohepatitis: A Review of Its Mechanism, Models and Medical Treatments.

Cheng Peng, Alastair G Stewart, Owen L Woodman, Rebecca H Ritchie, Cheng Xue Qin

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 146 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
146citing papers in PubMed, 4 pooled it
16.6field-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

146 citing papers in PubMed, 4 syntheses or guidelines pooled it, 223 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Trial
  6. Trial
  7. Trial
  8. Long-term hepatic safety of lomitapide in homozygous familial hypercholesterolaemia.Liver international : official journal of the International Association for the Study of the Liver · 2023
    Trial
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

86 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

5 authors at 3 institutions in 1 country.

Cheng PengDrug Discovery Biology, Monash Institute of Pharmaceutical Sciences, Melbourne, VIC, Australia.
Alastair G StewartDepartment of Pharmacology and Therapeutics, University of Melbourne, Melbourne, VIC, Australia.
Owen L WoodmanDrug Discovery Biology, Monash Institute of Pharmaceutical Sciences, Melbourne, VIC, Australia.
Rebecca H RitchieDrug Discovery Biology, Monash Institute of Pharmaceutical Sciences, Melbourne, VIC, Australia.
Cheng Xue QinDrug Discovery Biology, Monash Institute of Pharmaceutical Sciences, Melbourne, VIC, Australia.
Baker Heart and Diabetes Institute · AUAustralian Research Council · AUUniversity of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-alcoholic steatohepatitis (NASH) develops from non-alcoholic fatty liver disease (NAFLD). Currently, around 25% of the population is estimated to have NAFLD, and 25% of NAFLD patients are estimated to have NASH. NASH is typically characterized by liver steatosis inflammation, and fibrosis driven by metabolic disruptions such as obesity, diabetes, and dyslipidemia. NASH patients with significant fibrosis have increased risk of developing cirrhosis and liver failure. Currently, NASH is the second leading cause for liver transplant in the United States. More importantly, the risk of developing hepatocellular carcinoma from NASH has also been highlighted in recent studies. Patients may have NAFLD for years before progressing into NASH. Although the pathogenesis of NASH is not completely understood, the current "multiple-hits" hypothesis suggests that in addition to fat accumulation, elevated oxidative and ER stress may also drive liver inflammation and fibrosis. The development of clinically relevant animal models and pharmacological treatments for NASH have been hampered by the limited understanding of the disease mechanism and a lack of sensitive, non-invasive diagnostic tools. Currently, most pre-clinical animal models are divided into three main groups which includes: genetic models, diet-induced, and toxin + diet-induced animal models. Although dietary models mimic the natural course of NASH in humans, the models often only induce mild liver injury. Many genetic and toxin + diet-induced models rapidly induce the development of metabolic disruption and serious liver injury, but not without their own shortcomings. This review provides an overview of the "multiple-hits" hypothesis and an evaluation of the currently existing animal models of NASH. This review also provides an update on the available interventions for managing NASH as well as pharmacological agents that are currently undergoing clinical trials for the treatment of NASH.

Indexed as

animal modelsmetabolic syndromenon-alcoholic fatty liver diseasenon-alcoholic steatohepatitisobesitypharmacological treatmentssteatosis

Identifiers

PMID33343375
PMCPMC7745178
OpenAlexW3109853872

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.