Evidence map›Paper›PMID 32536770›Full record

ReviewWorld journal of gastroenterology2020

Metabolic inflammation as an instigator of fibrosis during non-alcoholic fatty liver disease.

Angeliki Katsarou, Ioannis I Moustakas, Iryna Pyrina, Panagiotis Lembessis, Michael Koutsilieris, Antonios Chatzigeorgiou

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in World journal of gastroenterology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed, 1 pooled it
9.6field-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

63 citing papers in PubMed, 1 synthesis or guideline pooled it, 89 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Insulin Resistance and Inflammation.International journal of molecular sciences · 2026
    Review
  9. Review
  10. Article
  11. Exercise Impacts Liver Disease: Balancing Metabolic and Immune Homeostasis.International journal of biological sciences · 2026
    Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Review
  19. Review
  20. Article

3 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

6 authors at 2 institutions in 2 countries.

Angeliki KatsarouDepartment of Physiology, Medical School, National and Kapodistrian University of Athens, Athens 11527, Greece.
Ioannis I MoustakasDepartment of Physiology, Medical School, National and Kapodistrian University of Athens, Athens 11527, Greece.
Iryna PyrinaInstitute for Clinical Chemistry and Laboratory Medicine, University Hospital and Faculty of Medicine Carl Gustav Carus of TU Dresden, Dresden 01307, Germany.
Panagiotis LembessisDepartment of Physiology, Medical School, National and Kapodistrian University of Athens, Athens 11527, Greece.
Michael KoutsilierisDepartment of Physiology, Medical School, National and Kapodistrian University of Athens, Athens 11527, Greece.
Antonios ChatzigeorgiouDepartment of Physiology, Medical School, National and Kapodistrian University of Athens, Athens 11527, Greece.
National and Kapodistrian University of Athens · GRTU Dresden · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-alcoholic fatty liver disease (NAFLD) is characterized by excessive storage of fatty acids in the form of triglycerides in hepatocytes. It is most prevalent in western countries and includes a wide range of clinical and histopathological findings, namely from simple steatosis to steatohepatitis and fibrosis, which may lead to cirrhosis and hepatocellular cancer. The key event for the transition from steatosis to fibrosis is the activation of quiescent hepatic stellate cells (qHSC) and their differentiation to myofibroblasts. Pattern recognition receptors (PRRs), expressed by a plethora of immune cells, serve as essential components of the innate immune system whose function is to stimulate phagocytosis and mediate inflammation upon binding to them of various molecules released from damaged, apoptotic and necrotic cells. The activation of PRRs on hepatocytes, Kupffer cells, the resident macrophages of the liver, and other immune cells results in the production of proinflammatory cytokines and chemokines, as well as profibrotic factors in the liver microenvironment leading to qHSC activation and subsequent fibrogenesis. Thus, elucidation of the inflammatory pathways associated with the pathogenesis and progression of NAFLD may lead to a better understanding of its pathophysiology and new therapeutic approaches.

Indexed as

AnimalsAnti-Inflammatory AgentsCell DifferentiationDiet, HealthyDisease Models, AnimalDisease ProgressionExercise TherapyGastrointestinal MicrobiomeHepatic Stellate CellsHumansInflammationInflammation MediatorsLiverLiver CirrhosisMyofibroblastsNon-alcoholic Fatty Liver DiseaseAnti-Inflammatory AgentsInflammation MediatorsHepatic stellate cellsInflammationLiver fibrosisNod-like receptorsNon-alcoholic fatty liver diseaseNon-alcoholic steatohepatitisToll-like receptors

Identifiers

PMID32536770
PMCPMC7267690
OpenAlexW3021086459

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.