Evidence map›Paper›PMID 31614491›Full record

ReviewInternational journal of molecular sciences2019

Development and Progression of Non-Alcoholic Fatty Liver Disease: The Role of Advanced Glycation End Products.

Dinali H Fernando, Josephine M Forbes, Peter W Angus, Chandana B Herath

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed, 5 pooled it
10.1field-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

99 citing papers in PubMed, 5 syntheses or guidelines pooled it, 178 citations in OpenAlex.

  1. Pooled it
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  5. Pooled it
  6. Trial
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  8. Review
  9. Article
  10. Article
  11. Unrevealing the Role of Flavonoids in Mitigation of Non-Alcoholic Fatty Liver Disease.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2026
    Review
  12. Frontiers in pharmacology · 2026
    Article
  13. Article
  14. Article
  15. Review
  16. Endoscopic sleeve gastrectomyWorld journal of gastrointestinal pharmacology and therapeutics · 2025
    Review
  17. Article
  18. Review
  19. Review
  20. Article

39 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

4 authors at 3 institutions in 1 country.

Dinali H FernandoDepartment of Medicine, The University of Melbourne, Melbourne 3084, Australia. hettiyaf@student.unimelb.edu.au.
Josephine M ForbesMater Institute, University of Queensland, Brisbane 4102, Australia. Josephine.Forbes@mater.uq.edu.au.
Peter W AngusLiver transplant unit, Austin Health, Heidelberg 3084, Australia. Peter.Angus@austin.org.au.
Chandana B HerathDepartment of Medicine, The University of Melbourne, Melbourne 3084, Australia. cherath@unimelb.edu.au.
University of Melbourne · AUAustin Health · AUUniversity of Queensland · AU

Funding

National Health and Medical Research Council APP1029990
6 · The paper itself

Abstract

Non-alcoholic fatty liver disease (NAFLD) affects up to 30% of the adult population and is now a major cause of liver disease-related premature illness and deaths in the world. Treatment is largely based on lifestyle modification, which is difficult to achieve in most patients. Progression of simple fatty liver or steatosis to its severe form non-alcoholic steatohepatitis (NASH) and liver fibrosis has been explained by a 'two-hit hypothesis'. Whilst simple steatosis is considered the first hit, its transformation to NASH may be driven by a second hit. Of several factors that constitute the second hit, advanced glycation end products (AGEs), which are formed when reducing-sugars react with proteins or lipids, have been implicated as major candidates that drive steatosis to NASH via the receptor for AGEs (RAGE). Both endogenous and processed food-derived (exogenous) AGEs can activate RAGE, mainly present on Kupffer cells and hepatic stellate cells, thus propagating NAFLD progression. This review focuses on the pathophysiology of NAFLD with special emphasis on the role of food-derived AGEs in NAFLD progression to NASH and liver fibrosis. Moreover, the effect of dietary manipulation to reduce AGE content in food or the therapies targeting AGE/RAGE pathway on disease progression is also discussed.

Indexed as

Disease ProgressionFoodGlycation End Products, AdvancedHepatic Stellate CellsHumansKupffer CellsNon-alcoholic Fatty Liver DiseaseReceptor for Advanced Glycation End ProductsGlycation End Products, AdvancedReceptor for Advanced Glycation End Productsadvanced glycation end productshepatic Kuppfer cellshepatic stellate cellsnon-alcoholic fatty liver diseaseoxidative stressreceptor for advanced glycation end products

Identifiers

PMID31614491
PMCPMC6834322
OpenAlexW2979736764

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.