Evidence map›Paper›PMID 32640349›Full record

ReviewFood and chemical toxicology : an international journal published for the British Industrial Biological Research Association2020

The liver fibrosis niche: Novel insights into the interplay between fibrosis-composing mesenchymal cells, immune cells, endothelial cells, and extracellular matrix.

Michitaka Matsuda, Ekihiro Seki

Open access · greenAbstract readReview
In one paragraph

Review in Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 7% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

  1. Pooled it
  2. Trial
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  6. Review
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  18. Challenges ofFrontiers in cell and developmental biology · 2025
    Review
  19. Article
  20. Pharmacotherapy of Liver Fibrosis and Hepatitis: Recent Advances.Pharmaceuticals (Basel, Switzerland) · 2024
    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

2 authors at 1 institution in 1 country.

Michitaka MatsudaDivision of Digestive and Liver Diseases, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA. Electronic address: michitaka.matsuda@cshs.org.
Ekihiro SekiDepartment of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, USA. Electronic address: ekihiro.seki@cshs.org.
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
NCI NIH HHS P01 CA233452NIAAA NIH HHS R01 AA027036NIDDK NIH HHS R01 DK085252
6 · The paper itself

Abstract

Liver fibrosis is a hepatic wound-healing response caused by chronic liver diseases that include viral hepatitis, alcoholic liver disease, non-alcoholic steatohepatitis, and cholestatic liver disease. Liver fibrosis eventually progresses to cirrhosis that is histologically characterized by an abnormal liver architecture that includes distortion of liver parenchyma, formation of regenerative nodules, and a massive accumulation of extracellular matrix (ECM). Despite intensive investigations into the underlying mechanisms of liver fibrosis, developments of anti-fibrotic therapies for liver fibrosis are still unsatisfactory. Recent novel experimental approaches, such as single-cell RNA sequencing and proteomics, have revealed the heterogeneity of ECM-producing cells (mesenchymal cells) and ECM-regulating cells (immune cells and endothelial cells). These approaches have accelerated the identification of fibrosis-specific subpopulations among these cell types. The ECM also consists of heterogenous components. Their production, degradation, deposition, and remodeling are dynamically regulated in liver fibrosis, further affecting the functions of cells responsible for fibrosis. These cellular and ECM elements cooperatively form a unique microenvironment: a fibrotic niche. Understanding the complex interplay between these elements could lead to a better understanding of underlying fibrosis mechanisms and to the development of effective therapies.

Indexed as

AnimalsEndothelial CellsExtracellular MatrixHumansLiver CirrhosisMesenchymal Stem CellsProteinsProteinsExtracellular matrixHepatic stellate cellsHyaluronic acidImmune cellsLiver sinusoidal endothelial cellsMyofibroblasts

Identifiers

PMID32640349
PMCPMC7484466
OpenAlexW3039317121

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.