Evidence map›Paper›PMID 30482910›Full record

ReviewNature reviews. Gastroenterology & hepatology2019

The role of macrophages in nonalcoholic fatty liver disease and nonalcoholic steatohepatitis.

Konstantin Kazankov, Simon Mark Dahl Jørgensen, Karen Louise Thomsen, Holger Jon Møller, Hendrik Vilstrup, Jacob George, Detlef Schuppan, Henning Grønbæk

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Gastroenterology & hepatology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 570 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
570citing papers in PubMed, 2 pooled it
42.8field-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

570 citing papers in PubMed, 2 syntheses or guidelines pooled it, 903 citations in OpenAlex.

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  6. Ethanol reshapes FFC-driven steatohepatitis through time-dependent fibrosis and lipid-droplet remodeling.American journal of physiology. Gastrointestinal and liver physiology · 2026
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510 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

8 authors at 3 institutions in 4 countries.

Konstantin KazankovDepartment of Hepatology and Gastroenterology, Aarhus University Hospital, Aarhus, Denmark. konskaza@rm.dk.
Simon Mark Dahl JørgensenDepartment of Hepatology and Gastroenterology, Aarhus University Hospital, Aarhus, Denmark.ORCID http://orcid.org/0000-0002-5135-7435
Karen Louise ThomsenDepartment of Hepatology and Gastroenterology, Aarhus University Hospital, Aarhus, Denmark.
Holger Jon MøllerDepartment of Clinical Biochemistry, Aarhus University Hospital, Aarhus, Denmark.
Hendrik VilstrupDepartment of Hepatology and Gastroenterology, Aarhus University Hospital, Aarhus, Denmark.
Jacob GeorgeStorr Liver Centre, The Westmead Institute for Medical Research, University of Sydney and Westmead Hospital, Westmead, New South Wales, Australia.
Detlef Schuppan *Institute of Translational Immunology and Research Center for Immunology, University Medical Center, Johannes-Gutenberg-University, Mainz, Germany.
Henning Grønbæk *Department of Hepatology and Gastroenterology, Aarhus University Hospital, Aarhus, Denmark.
Aarhus University Hospital · DKBeth Israel Deaconess Medical Center · USThe University of Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nonalcoholic fatty liver disease (NAFLD) and its inflammatory and often progressive subtype nonalcoholic steatohepatitis (NASH) are becoming the leading cause of liver-related morbidity and mortality worldwide, and a primary indication for liver transplantation. The pathophysiology of NASH is multifactorial and not yet completely understood; however, innate immunity is a major contributing factor in which liver-resident macrophages (Kupffer cells) and recruited macrophages play a central part in disease progression. In this Review, we assess the evidence for macrophage involvement in the development of steatosis, inflammation and fibrosis in NASH. In this process, not only the polarization of liver macrophages towards a pro-inflammatory phenotype is important, but adipose tissue macrophages, especially in the visceral compartment, also contribute to disease severity and insulin resistance. Macrophage activation is mediated by factors such as endotoxins and translocated bacteria owing to increased intestinal permeability, factors released from damaged or lipoapoptotic hepatocytes, as well as alterations in gut microbiota and defined nutritional components, including certain free fatty acids, cholesterol and their metabolites. Reflecting the important role of macrophages in NASH, we also review studies investigating drugs that target macrophage recruitment to the liver, macrophage polarization and their inflammatory effects as potential treatment options for patients with NASH.

Indexed as

AnimalsDisease ProgressionHumansLiverMacrophagesNon-alcoholic Fatty Liver Disease

Identifiers

PMID30482910
OpenAlexW2902538813

What OpenQuestion holds

Textmetadata
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.