Evidence map›Paper›PMID 30405618›Full record

ReviewFrontiers in immunology2018

Adapted Immune Responses of Myeloid-Derived Cells in Fatty Liver Disease.

Jana Hundertmark, Oliver Krenkel, Frank Tacke

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 8% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
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  7. Review
  8. Toxicity and efficacy study of a combination of two retinoic acids in an ApoE knockout mouse model of atherosclerosis.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
    Article
  9. Review
  10. Article
  11. Experimental model and novel therapeutic targets for non-alcoholic fatty liver disease development.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2023
    Review
  12. Review
  13. Article
  14. Article
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  16. Review
  17. Roles of Macrophages in the Development and Treatment of Gut Inflammation.Frontiers in cell and developmental biology · 2021
    Review
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  19. Article
  20. Article
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

3 authors at 1 institution in 1 country.

Jana HundertmarkDepartment of Medicine III, University Hospital Aachen, Aachen, Germany.
Oliver KrenkelDepartment of Medicine III, University Hospital Aachen, Aachen, Germany.
Frank TackeDepartment of Medicine III, University Hospital Aachen, Aachen, Germany.
Universitätsklinikum Aachen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-alcoholic fatty liver disease (NAFLD) is considered to be one of the most frequent chronic liver diseases worldwide and is associated with an increased risk of developing liver cirrhosis and hepatocellular carcinoma. Hepatic macrophages, mainly comprising monocyte derived macrophages and tissue resident Kupffer cells, are characterized by a high diversity and plasticity and act as key regulators during NAFLD progression, in conjunction with other infiltrating myeloid cells like neutrophils or dendritic cells. The activation and polarization of myeloid immune cells is influenced by dietary components, inflammatory signals like danger-associated molecular patterns (DAMPs) or cytokines as well as gut-derived inflammatory factors such as pathogen-associated molecular patterns (PAMPs). The functionality of myeloid leukocytes in the liver is directly linked to their inflammatory polarization, which is shaped by local and systemic inflammatory mediators such as cytokines, chemokines, PAMPs, and DAMPs. These environmental signals provoke intracellular adaptations in myeloid cells, including inflammasome and transcription factor activation, inflammatory signaling pathways, or switches in cellular metabolism. Dietary changes and obesity also promote a dysbalance in intestinal microbiota, which can facilitate intestinal permeability and bacterial translocation. The aim of this review is to highlight recent findings on the activating pathways of innate immune cells during the progression of NAFLD, dissecting local hepatic and systemic signals, dietary and metabolic factors as well as pathways of the gut-liver axis. Understanding the mechanism by which plasticity of myeloid-derived leukocytes is related to metabolic changes and NAFLD progression may provide options for new therapeutic approaches.

Indexed as

Adaptive ImmunityAnimalsBiomarkersCell DifferentiationEnergy MetabolismHumansImmunity, InnateImmunomodulationMacrophagesMyeloid CellsMyeloid-Derived Suppressor CellsNon-alcoholic Fatty Liver DiseaseOrgan SpecificityBiomarkersfibrosisinnate immunitylipotoxicitymacrophagesmetabolismNASHPAMPssteatosis

Identifiers

PMID30405618
PMCPMC6200865
OpenAlexW2896975388

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.