Evidence map›Paper›PMID 39008791›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2024

Cutting Edge: Hepatic Stellate Cells Drive the Phenotype of Monocyte-derived Macrophages to Regulate Liver Fibrosis in Metabolic Dysfunction-associated Steatohepatitis.

Mandy M Chan, Li He, Brian N Finck, Joel D Schilling, Sabine Daemen

Abstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
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

6 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. 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.

Mandy M ChanDepartment of Internal Medicine, Washington University School of Medicine, St. Louis, MO.ORCID 0000-0001-6511-0962
Li HeDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO.
Brian N FinckDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO.ORCID 0000-0001-5411-3674
Joel D SchillingDepartment of Internal Medicine, Washington University School of Medicine, St. Louis, MO.ORCID 0000-0002-3884-1994
Sabine DaemenDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO.ORCID 0000-0002-2811-8145

Funding

Washington University Nutrition Obesity Research CenterP30DK056341 · NIDDK · WASHINGTON UNIVERSITY · PI Dominic N Reeds · 1999 to 2026
$30.2M
Harnessing macrophage lysosomal lipid metabolism in obesity-associated diseasesR01DK131188 · NIDDK · WASHINGTON UNIVERSITY · PI MITTENDORFER, BETTINA, RAZANI, BABAK · 2022 to 2025
$2.6M
MACROPHAGE METABOLISM AND INFLAMMATION IN METABOLIC DISEASER01DK110034 · NIDDK · WASHINGTON UNIVERSITY · PI SCHILLING, JOEL DAVID · 2016 to 2020
$1.7M
HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) R01DK13118801HHS | NIH | NIDDK | Division of Diabetes, Endocrinology, and Metabolic Diseases (DEM) R01 DK11003401NIDDK NIH HHS P30 DK056341NIDDK NIH HHS R01 DK110034NIDDK NIH HHS R01 DK131188
6 · The paper itself

Abstract

Metabolic dysfunction-associated steatohepatitis (MASH) is characterized by infiltration of monocyte-derived macrophages (MdMs) into the liver; however, the function of these macrophages is largely unknown. We previously demonstrated that a population of MdMs, referred to as hepatic lipid-associated macrophages (LAMs), assemble into aggregates termed hepatic crown-like structures in areas of liver fibrosis. Intriguingly, decreasing MdM recruitment resulted in increased liver fibrosis, suggesting that LAMs contribute to antifibrotic pathways in MASH. In this study, we determined that hepatic crown-like structures are characterized by intimate interactions between activated hepatic stellate cells (HSCs) and macrophages in a collagen matrix in a mouse model of MASH. MASH macrophages displayed collagen-degrading capacities, and HSCs derived from MASH livers promoted expression of LAM marker genes and acquisition of a collagen-degrading phenotype in naive macrophages. These data suggest that crosstalk between HSCs and macrophages may contribute to collagen degradation MASH.

Indexed as

Hepatic Stellate CellsLiver CirrhosisMacrophagesPhenotypeAnimalsCollagenDisease Models, AnimalFatty LiverHumansLiverMaleMiceMice, Inbred C57BLCollagen

Identifiers

PMID39008791
PMCPMC11254326

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Registered trials

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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.