Evidence map›Paper›PMID 26939970›Full record

ReviewJournal of gastroenterology2016

Hepatic sinusoids in liver injury, inflammation, and fibrosis: new pathophysiological insights.

Thomas Greuter, Vijay H Shah

Open access · bronzeAbstract readReview
PubMed Publisher
In one paragraph

Review in Journal of gastroenterology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
12.6field-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

64 citing papers in PubMed, 138 citations in OpenAlex.

  1. Trial
  2. Lumped parameter modeling of changes in liver hemodynamics due to cirrhosis.Biomechanics and modeling in mechanobiology · 2026
    Article
  3. Review
  4. Review
  5. The Cardiohepatic Axis in Heart Failure.JACC. Basic to translational science · 2025
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. [Research progress of liver sinusoidal endothelial cells in nonalcoholic fatty liver disease].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2023
    Review

4 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 2 institutions in 2 countries.

Thomas GreuterDivision of Gastroenterology and Hepatology, University Hospital Zurich, Zurich, Switzerland.
Vijay H ShahGastroenterology Research Unit, Department of Gastroenterology and Hepatology, Mayo Clinic and Foundation, 200 First St. SW, Rochester, MN, 55905, USA. shah.vijay@mayo.edu.
Mayo Clinic · USUniversity Hospital of Zurich · CH

Funding

Molecular Mechanisms of Portal HypertensionR01DK059615 · NIDDK · MAYO CLINIC ROCHESTER · PI SHAH, VIJAY H. · 2002 to 2023
$6.4M
NIDDK NIH HHS R01 DK059615
6 · The paper itself

Abstract

Changes of hepatic sinusoids are crucial in the pathogenesis of liver cirrhosis and portal hypertension. Liver injury leads to distinct morphological abnormalities such as loss of sinusoidal fenestration, vasoconstriction, and angiogenesis as well as molecular changes. Communication between the two key cells in this hepatic microenvironment-hepatic stellate cells (HSC) and sinusoidal endothelial cells (SEC)-has been studied for many years and several canonical pathways have been elucidated, such as decreased eNOS activity or increased PDGF and TGF-β production leading to activation and migration of HSC. In recent studies, alternative pathways of intercellular communication in liver diseases have been described such as cell-derived extracellular vesicles called exosomes, which deliver cell compounds to their target cells. Moreover, such extracellular vesicles may link injury to inflammation in alcoholic hepatitis. While inflammation leading to liver fibrosis has been studied in detail, in some circumstances pathways other than the known canonical inflammatory pathways may contribute to hepatic fibrogenesis. For example, in congestive hepatopathy, sinusoidal dilatation and fibrosis have been shown to be mediated by non-inflammatory mechanisms and associated with sinusoidal thrombi. A recently developed murine model further enables experimental studies of this disease entity. Increasing knowledge about these alternative disease pathways in liver injury, inflammation, and fibrosis may reveal possible target molecules for future therapies. This article builds upon a seminar given at the recent 3rd JSGE International Topic Conference in Sendai, Japan, and reviews the areas outlined above.

Indexed as

CapillariesCell CommunicationEndothelial CellsHepatic Stellate CellsHumansLiver DiseasesExosome signalingHepatic stellate cellIntercellular communicationIntrasinusoidal thrombosisMicrovesiclesSinusoidal epithelial cell

Identifiers

PMID26939970
OpenAlexW2290962805

What OpenQuestion holds

Textmetadata
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.