Evidence map›Paper›PMID 36691794›Full record

ReviewBioscience reports2023

Inflammatory processes involved in NASH-related hepatocellular carcinoma.

Stefania Cannito, Umberto Dianzani, Maurizio Parola, Emanuele Albano, Salvatore Sutti

Open access · goldAbstract readReview
In one paragraph

Review in Bioscience reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
5.8field-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

17 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
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  3. Article
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  5. Molecular mechanisms in MASLD/MASH-related HCC.Hepatology (Baltimore, Md.) · 2025
    Review
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  11. Article
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  16. Metabolic Reprogramming of HCC: A New Microenvironment for Immune Responses.International journal of molecular sciences · 2023
    Review
  17. Review
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 2 institutions in 1 country.

Stefania CannitoDepartment of Clinical and Biological Sciences, Unit of Experimental Medicine and Clinical Pathology, University of Turin, Turin, Italy.
Umberto DianzaniDepartment of Health Sciences and Interdisciplinary Research Centre for Autoimmune Diseases, University of East Piedmont, Novara, Italy.
Maurizio ParolaDepartment of Clinical and Biological Sciences, Unit of Experimental Medicine and Clinical Pathology, University of Turin, Turin, Italy.
Emanuele AlbanoDepartment of Health Sciences and Interdisciplinary Research Centre for Autoimmune Diseases, University of East Piedmont, Novara, Italy.ORCID 0000-0003-4738-7049
Salvatore SuttiDepartment of Health Sciences and Interdisciplinary Research Centre for Autoimmune Diseases, University of East Piedmont, Novara, Italy.
Università degli Studi del Piemonte Orientale “Amedeo Avogadro” · ITUniversity of Turin · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is the fourth leading cause of cancer-related death worldwide. In the recent years nonalcoholic fatty liver disease (NAFLD) is becoming a growing cause of HCCs and the incidence of NAFLD-related HCCs is expected to further dramatically increase by the next decade. Chronic inflammation is regarded as the driving force of NAFLD progression and a key factor in hepatic carcinogenesis. Hepatic inflammation in NAFLD results from the persistent stimulation of innate immunity in response to hepatocellular injury and gut dysbiosis as well as by the activation of adaptive immunity. However, the relative roles of innate and adaptive immunity in the processes leading to HCC are still incompletely characterized. This is due to the complex interplay between different liver cell populations, which is also strongly influenced by gut-derived bacterial products, metabolic/nutritional signals. Furthermore, carcinogenic mechanisms in NAFLD/NASH appear to involve the activation of signals mediated by hypoxia inducible factors. This review discusses recent data regarding the contribution of different inflammatory cells to NAFLD-related HCC and their possible impact on patient response to current treatments.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsNon-alcoholic Fatty Liver DiseaseHumansInflammationHepatocellular carcinomaLiver inflammationlymphocytesNonalcoholic steatohepatitis

Identifiers

PMID36691794
PMCPMC9874450
OpenAlexW4317871456

What Socratic 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 Socratic graph.