Evidence map›Paper›PMID 36907380›Full record

ReviewCellular and molecular gastroenterology and hepatology2023

The Multifaceted Roles of Macrophages in NAFLD Pathogenesis.

Joscha Vonderlin, Triantafyllos Chavakis, Michael Sieweke, Frank Tacke

Open access · goldAbstract readReview
In one paragraph

Review in Cellular and molecular gastroenterology and hepatology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
17.4field-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

67 citing papers in PubMed, 82 citations in OpenAlex.

  1. Reprogramming macrophages to treat liver diseases.Hepatology (Baltimore, Md.) · 2026
    Review
  2. Article
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  5. [SingleZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026
    Article
  6. Review
  7. Article
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  11. Review
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  14. Macrophage Plg-RJournal of thrombosis and haemostasis : JTH · 2026
    Article
  15. TREM2-expressing macrophages in liver diseases.Trends in endocrinology and metabolism: TEM · 2026
    Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review

7 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 2 institutions in 1 country.

Joscha VonderlinDepartment of Hepatology and Gastroenterology, Charité-Universitätsmedizin Berlin, Campus Virchow-Klinikum and Campus Charité Mitte, Berlin, Germany.
Triantafyllos ChavakisInstitute for Clinical Chemistry and Laboratory Medicine, University Hospital, Faculty of Medicine Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.
Michael SiewekeCenter for Regenerative Therapies Dresden, Technische Universität Dresden, Dresden, Germany.
Frank TackeDepartment of Hepatology and Gastroenterology, Charité-Universitätsmedizin Berlin, Campus Virchow-Klinikum and Campus Charité Mitte, Berlin, Germany. Electronic address: frank.tacke@charite.de.
Charité - Universitätsmedizin Berlin · DETU Dresden · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nonalcoholic fatty liver disease (NAFLD) is the liver manifestation of the metabolic syndrome. NAFLD constitutes a spectrum of pathologies ranging from simple hepatic steatosis (nonalcoholic fatty liver) to the more progressive form of steatohepatitis and fibrosis, which can culminate in liver cirrhosis and hepatocellular carcinoma. Macrophages play multiple roles in the context of NAFLD pathogenesis by regulating inflammatory responses and metabolic homeostasis in the liver and thereby may represent an attractive therapeutic target. Advances in high-resolution methods have highlighted the extraordinary heterogeneity and plasticity of hepatic macrophage populations and activation states thereof. Harmful/disease-promoting as well as beneficial/restorative macrophage phenotypes co-exist and are dynamically regulated, thus this complexity must be taken into consideration in strategies concerning therapeutic targeting. Macrophage heterogeneity in NAFLD includes their distinct ontogeny (embryonic Kupffer cells vs bone marrow-/monocyte-derived macrophages) as well as their functional phenotype, for example, inflammatory phagocytes, lipid- and scar-associated macrophages, or restorative macrophages. Here, we discuss the multifaceted role of macrophages in the pathogenesis of NAFLD in steatosis, steatohepatitis, and transition to fibrosis and hepatocellular carcinoma, focusing on both their beneficial and maladaptive functions at different disease stages. We also highlight the systemic aspect of metabolic dysregulation and illustrate the contribution of macrophages in the reciprocal crosstalk between organs and compartments (eg, the gut-liver axis, adipose tissue, and cardiohepatic metabolic interactions). Furthermore, we discuss the current state of development of pharmacologic treatment options targeting macrophage biology.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsNon-alcoholic Fatty Liver DiseaseFibrosisHumansMacrophagesHCCliver fibrosismacrophageNASHobesitytype 2 diabetes

Identifiers

PMID36907380
PMCPMC10148157
OpenAlexW4323817405

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.