Evidence map›Paper›PMID 32089540›Full record

ArticleCells2020

Antifibrotic Effects of Amyloid-Beta and Its Loss in Cirrhotic Liver.

Gayane Hrachia Buniatian, Ralf Weiskirchen, Thomas S Weiss, Ute Schwinghammer, Martin Fritz, Torgom Seferyan, Barbara Proksch, Michael Glaser, Ali Lourhmati, Marine Buadze and 13 more

Open access · goldAbstract read
In one paragraph

Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

8 citing papers in PubMed, 13 citations in OpenAlex.

  1. Therapeutic Potential of Ellagic Acid in Liver Diseases.Molecules (Basel, Switzerland) · 2025
    Review
  2. Article
  3. Consequences of Amyloid-β Deficiency for the Liver.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. 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

23 authors at 11 institutions in 4 countries.

Gayane Hrachia BuniatianDepartment of Clinical Pharmacology, University Hospital of Tübingen, 72076 Tübingen, Germany.
Ralf WeiskirchenInstitute of Molecular Pathobiochemistry, Experimental Gene Therapy and Clinical Chemistry, RWTH University Hospital Aachen, 52074 Aachen, Germany.ORCID 0000-0003-3888-0931
Thomas S WeissChildren's University Hospital (KUNO), University of Regensburg, 93053 Regensburg, Germany.ORCID 0000-0003-0336-0581
Ute SchwinghammerDepartment of Clinical Pharmacology, University Hospital of Tübingen, 72076 Tübingen, Germany.
Martin FritzDepartment of Clinical Pharmacology, University Hospital of Tübingen, 72076 Tübingen, Germany.
Torgom SeferyanH. Buniatian Institute of Biochemistry, National Academy of Sciences of the Republic of Armenia (NAS RA), Yerevan 0014, Armenia.
Barbara ProkschDepartment of Clinical Pharmacology, University Hospital of Tübingen, 72076 Tübingen, Germany.
Michael GlaserDepartment of Clinical Pharmacology, University Hospital of Tübingen, 72076 Tübingen, Germany.
Ali LourhmatiDepartment of Clinical Pharmacology, University Hospital of Tübingen, 72076 Tübingen, Germany.
Marine BuadzeDepartment of Clinical Pharmacology, University Hospital of Tübingen, 72076 Tübingen, Germany.
Erawan Borkham-KamphorstInstitute of Molecular Pathobiochemistry, Experimental Gene Therapy and Clinical Chemistry, RWTH University Hospital Aachen, 52074 Aachen, Germany.
Frank GaunitzDepartment of Neurosurgery, University Hospital of Leipzig, 04103 Leipzig, Germany.ORCID 0000-0001-6628-0605
Christoph H GleiterDepartment of Clinical Pharmacology, University Hospital of Tübingen, 72076 Tübingen, Germany.
Thomas LangDr. Margarete Fischer-Bosch Institute of Clinical Pharmacology, 70376 Stuttgart, Germany, and University of Tuebingen, 72076 Tuebingen, Germany.
Elke SchaeffelerDr. Margarete Fischer-Bosch Institute of Clinical Pharmacology, 70376 Stuttgart, Germany, and University of Tuebingen, 72076 Tuebingen, Germany.
Roman TremmelDr. Margarete Fischer-Bosch Institute of Clinical Pharmacology, 70376 Stuttgart, Germany, and University of Tuebingen, 72076 Tuebingen, Germany.ORCID 0000-0003-1564-0433
Holger CynisDepartment of Drug Design and Target Validation, Fraunhofer Institute for Cell Therapy and Immunology, 06120 Halle, Germany.
William H FreyCenter for Memory & Aging, HealthPartners Neuroscience Center, St. Paul, MN 55130, USA.ORCID 0000-0002-6373-0794
Rolf GebhardtRudolf-Schönheimer Institute of Biochemistry, Faculty of Medicine, University of Leipzig, 04103 Leipzig, Germany.
Scott L FriedmanDivision of Liver Diseases, Icahn School of Medicine at Mount Sinai, New York, NY 10029-6574, USA.ORCID 0000-0003-1178-6195
Wolfgang MikulitsDepartment of Medicine I, Institute of Cancer Research, Comprehensive Cancer Center, Medical University of Vienna, Vienna 1090, Austria.ORCID 0000-0003-4612-7106
Matthias SchwabDepartment of Clinical Pharmacology, University Hospital of Tübingen, 72076 Tübingen, Germany.
Lusine DanielyanDepartment of Clinical Pharmacology, University Hospital of Tübingen, 72076 Tübingen, Germany.
University Children's Hospital Tübingen · DEDr. Margarete Fischer-Bosch-Institute of Clinical Pharmacology · DEH.Buniatian Institute of Biochemistry · AMUniversitätsklinikum Aachen · DEComprehensive Cancer Center Vienna · ATFraunhofer Institute for Cell Therapy and Immunology · DEHealthPartners · USIcahn School of Medicine at Mount Sinai · USLeipzig University · DEUniversity Hospital Leipzig · DEUniversity Hospital Regensburg · DE

Funding

Austrian Science Fund FWF P 31720
6 · The paper itself

Abstract

The function and regulation of amyloid-beta (Aβ) in healthy and diseased liver remains unexplored. Because Aβ reduces the integrity of the blood-brain barrier we have examined its potential role in regulating the sinusoidal permeability of normal and cirrhotic liver. Aβ and key proteins that generate (beta-secretase 1 and presenilin-1) and degrade it (neprilysin and myelin basic protein) were decreased in human cirrhotic liver. In culture, activated hepatic stellate cells (HSC) internalized Aβ more efficiently than astrocytes and HSC degraded Aβ leading to suppressed expression of α-smooth muscle actin (α-SMA), collagen 1 and transforming growth factor β (TGFβ). Aβ also upregulated sinusoidal permeability marker endothelial NO synthase (eNOS) and decreased TGFβ in cultured human liver sinusoidal endothelial cells (hLSEC). Liver Aβ levels also correlate with the expression of eNOS in transgenic Alzheimer's disease mice and in human and rodent cirrhosis/fibrosis. These findings suggest a previously unexplored role of Aβ in the maintenance of liver sinusoidal permeability and in protection against cirrhosis/fibrosis via attenuation of HSC activation.

Indexed as

Amyloid beta-PeptidesAnimalsDisease Models, AnimalFibrosisGene ExpressionHumansLiver CirrhosisMaleMiceMice, TransgenicMiddle AgedPeptide FragmentsRatsRats, Sprague-DawleyAmyloid beta-Peptidesamyloid beta-protein (1-34)Peptide FragmentsAlzheimer’s diseaseastrocytesbeta secretaseendothelial nitric oxide synthasehepatic stellate cellsliver cirrhosisliver sinusoidal endothelial cellsliver sinusoidal permeabilitymyelin basic proteinneprilysinpresenilin

Identifiers

PMID32089540
PMCPMC7072823
OpenAlexW3006576527

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.