Evidence map›Paper›PMID 36159810›Full record

ArticleFrontiers in immunology2022

Hepatic damage caused by long-term high cholesterol intake induces a dysfunctional restorative macrophage population in experimental NASH.

Ana C Maretti-Mira, Matthew P Salomon, Angela M Hsu, Gary C Kanel, Lucy Golden-Mason

Abstract read
In one paragraph

Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
–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

13 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Article
  4. Cholesterol-containing lipid crystals can directly stiffen the rat steatotic liver before fibrosis.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  5. Article
  6. Article
  7. Synbiotic Administration of d-Tagatose andFood science & nutrition · 2025
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. 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

5 authors.

Ana C Maretti-MiraUSC Research Center for Liver Disease, Keck School of Medicine, University of Southern California, Los Angeles, CA, United States.
Matthew P SalomonUSC Research Center for Liver Disease, Keck School of Medicine, University of Southern California, Los Angeles, CA, United States.
Angela M HsuUSC Research Center for Liver Disease, Keck School of Medicine, University of Southern California, Los Angeles, CA, United States.
Gary C KanelUSC Research Center for Liver Disease, Keck School of Medicine, University of Southern California, Los Angeles, CA, United States.
Lucy Golden-MasonUSC Research Center for Liver Disease, Keck School of Medicine, University of Southern California, Los Angeles, CA, United States.

Funding

USC RESEARCH CENTER FOR LIVER DISEASES: PILOT PROGRAMSP30DK048522 · NIDDK · UNIVERSITY OF SOUTHERN CALIFORNIA · PI KAPLOWITZ, NEIL · 1995 to 2020
$21.8M
Human Group 2 Innate Lympohocyte Cell (ILC2) populations contribute to Hepatic FibrosisR01DK106491 · NIDDK · UNIVERSITY OF SOUTHERN CALIFORNIA · PI GOLDEN, LUCY MARY · 2015 to 2019
$1.8M
Innate Immunity, Cholesterol, and NASH PathogenesisR01DK117004 · NIDDK · UNIVERSITY OF SOUTHERN CALIFORNIA · PI GOLDEN, LUCY MARY · 2020 to 2023
$1.5M
NIDDK NIH HHS P30 DK048522NIDDK NIH HHS R01 DK106491NIDDK NIH HHS R01 DK117004
6 · The paper itself

Abstract

Excessive dietary cholesterol is preferentially stored in the liver, favoring the development of nonalcoholic steatohepatitis (NASH), characterized by progressive hepatic inflammation and fibrosis. Emerging evidence indicates a critical contribution of hepatic macrophages to NASH severity. However, the impact of cholesterol on these cells in the setting of NASH remains elusive. Here, we demonstrate that the dietary cholesterol content directly affects hepatic macrophage global gene expression. Our findings suggest that the modifications triggered by prolonged high cholesterol intake induce long-lasting hepatic damage and support the expansion of a dysfunctional pro-fibrotic restorative macrophage population even after cholesterol reduction. The present work expands the understanding of the modulatory effects of cholesterol on innate immune cell transcriptome and may help identify novel therapeutic targets for NASH intervention.

Indexed as

HypercholesterolemiaNon-alcoholic Fatty Liver DiseaseAnimalsCholesterolCholesterol, DietaryDisease Models, AnimalHumansMacrophagesCholesterolCholesterol, Dietarycholesterolinnate immunityKupffer cellsnonalcoholic fatty liver disease (NAFLD)RNAseqtissue macrophages

Identifiers

PMID36159810
PMCPMC9495937

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.