Evidence map›Paper›PMID 32242330›Full record

ReviewSeminars in liver disease2020

Hepatic Stellate Cell-Macrophage Crosstalk in Liver Fibrosis and Carcinogenesis.

Michitaka Matsuda, Ekihiro Seki

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in liver disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
115citing papers in PubMed, 1 pooled it
9.8field-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

115 citing papers in PubMed, 1 synthesis or guideline pooled it, 167 citations in OpenAlex.

  1. Pooled it
  2. E3 Ubiquitin Ligases in MASH-Associated Liver Fibrosis: Mechanisms and Therapeutic Opportunities.Liver international : official journal of the International Association for the Study of the Liver · 2026
    Review
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  7. From Theory to Practice: Which Biomarkers Are Ready for Predicting Response in Advanced HCC?Liver international : official journal of the International Association for the Study of the Liver · 2026
    Review
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55 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

2 authors at 1 institution in 1 country.

Michitaka MatsudaDivision of Digestive and Liver Diseases, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California.
Ekihiro SekiDivision of Digestive and Liver Diseases, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California.
Cedars-Sinai Medical Center · US

Funding

The paradoxical roles of beta hydroxy butyrate in the liver pro-metastatic nicheP01CA233452 · NCI · CEDARS-SINAI MEDICAL CENTER · PI BHOWMICK, NEIL A., LU, SHELLY CHI-LOO · 2020 to 2024
$9.5M
LPS binding to TLR4 regulates hepatic stellate cell activation and fibrosisR01DK085252 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI EKIHIRO SEKI · 2011 to 2026
$4.8M
Role of TLR7 in progression and treatment of alcoholic hepatitisR01AA027036 · NIAAA · CEDARS-SINAI MEDICAL CENTER · PI SEKI, EKIHIRO · 2018 to 2022
$2.1M
Alcohol enhances colon cancer liver metastasis via cancer-associated fibroblastsR21AA025841 · NIAAA · CEDARS-SINAI MEDICAL CENTER · PI SEKI, EKIHIRO · 2017 to 2018
$459k
NCI NIH HHS P01 CA233452NIAAA NIH HHS R01 AA027036NIAAA NIH HHS R21 AA025841NIDDK NIH HHS R01 DK085252P01CA233452 National Institutes of HealthR01AA027036 National Institutes of HealthR01DK085252 National Institutes of HealthR21AA025841 National Institutes of Health
6 · The paper itself

Abstract

Chronic liver injury due to viral hepatitis, alcohol abuse, and metabolic disorders is a worldwide health concern. Insufficient treatment of chronic liver injury leads to fibrosis, causing liver dysfunction and carcinogenesis. Most cases of hepatocellular carcinoma (HCC) develop in the fibrotic liver. Pathological features of liver fibrosis include extracellular matrix (ECM) accumulation, mesenchymal cell activation, immune deregulation, and angiogenesis, all of which contribute to the precancerous environment, supporting tumor development. Among liver cells, hepatic stellate cells (HSCs) and macrophages play critical roles in fibrosis and HCC. These two cell types interplay and remodel the ECM and immune microenvironment in the fibrotic liver. Once HCC develops, HCC-derived factors influence HSCs and macrophages to switch to protumorigenic cell populations, cancer-associated fibroblasts and tumor-associated macrophages, respectively. This review aims to summarize currently available data on the roles of HSCs and macrophages in liver fibrosis and HCC, with a focus on their interaction.

Indexed as

AnimalsCarcinogenesisCarcinoma, HepatocellularCell CommunicationHepatic Stellate CellsHumansKupffer CellsLiver CirrhosisLiver NeoplasmsTumor Microenvironment

Identifiers

PMID32242330
PMCPMC7484001
OpenAlexW3014902879

What OpenQuestion holds

Textmetadata
LicenceTDM
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.