Evidence map›Paper›PMID 35036886›Full record

ArticleJHEP reports : innovation in hepatology2022

Vasoconstrictor antagonism improves functional and structural vascular alterations and liver damage in rats with early NAFLD.

Denise van der Graaff, Shivani Chotkoe, Benedicte De Winter, Joris De Man, Christophe Casteleyn, Jean-Pierre Timmermans, Isabel Pintelon, Luisa Vonghia, Wilhelmus J Kwanten, Sven Francque

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in JHEP reports : innovation in hepatology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

18 citing papers in PubMed, 37 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 1 institution in 3 countries.

Denise van der GraaffDepartment of Gastroenterology and Hepatology, Antwerp University Hospital, Antwerp, Belgium.
Shivani ChotkoeDepartment of Gastroenterology and Hepatology, Antwerp University Hospital, Antwerp, Belgium.
Benedicte De WinterDepartment of Gastroenterology and Hepatology, Antwerp University Hospital, Antwerp, Belgium.
Joris De ManLaboratory of Experimental Medicine and Pediatrics (LEMP), Division of Gastroenterology-Hepatology, Faculty of Medicine and Health Sciences, University of Antwerp, Antwerp, Belgium.
Christophe CasteleynDepartment of Morphology, Faculty of Veterinary Medicine, Ghent University, Ghent, Belgium.
Jean-Pierre TimmermansLaboratory of Cell Biology and Histology, Antwerp Centre for Advanced Microscopy (ACAM), University of Antwerp, Antwerp, Belgium.
Isabel PintelonLaboratory of Cell Biology and Histology, Antwerp Centre for Advanced Microscopy (ACAM), University of Antwerp, Antwerp, Belgium.
Luisa VonghiaDepartment of Gastroenterology and Hepatology, Antwerp University Hospital, Antwerp, Belgium.
Wilhelmus J KwantenDepartment of Gastroenterology and Hepatology, Antwerp University Hospital, Antwerp, Belgium.
Sven FrancqueDepartment of Gastroenterology and Hepatology, Antwerp University Hospital, Antwerp, Belgium.
University of Antwerp · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND &

aimsIntrahepatic vascular resistance is increased in early non-alcoholic fatty liver disease (NAFLD), potentially leading to tissue hypoxia and triggering disease progression. Hepatic vascular hyperreactivity to vasoconstrictors has been identified as an underlying mechanism. This study investigates vasoconstrictive agonism and antagonism in 2 models of early NAFLD and in non-alcoholic steatohepatitis (NASH).

methodsThe effects of endothelin-1 (ET-1), angiotensin II (ATII) and thromboxane A

resultsThe THPG and consequent portal pressure were significantly increased in both models of steatosis and in NASH. ET-1, ATII and TxA

conclusionsAntagonism of vasoconstrictive mediators improves intrahepatic vascular function. Both ET-1 and ATII antagonists showed additional benefit and bosentan even mitigated steatosis and structural liver damage. In conclusion, vasoconstrictive antagonism is a potentially promising therapeutic option for the treatment of early NAFLD. LAY SUMMARY: In non-alcoholic fatty liver disease (NAFLD), hepatic blood flow is impaired and the blood pressure in the liver blood vessels is increased as a result of an increased response of the liver vasculature to vasoconstrictors. Using drugs to block the constriction of the intrahepatic vasculature, the resistance of the liver blood vessels decreases and the increased portal pressure is reduced. Moreover, blocking the vasoconstrictive endothelin-1 pathway restored parenchymal architecture and reduced disease severity.

Indexed as

ALT, alanine aminotransferaseangiotensin IIARB, angiotensin receptor blockerAST, aspartate aminotransferaseATII, angiotensin IICOX, cyclooxygenaseendothelin-1ET, endothelinHFHFD, high-fat high-fructose dietIHVR, intrahepatic vascular resistanceJak2, Janus-kinase-2MCD, methionine-choline deficient dietMx, methoxamineNAFLD, non-alcoholic fatty liver diseaseNASH, non-alcoholic steatohepatitisnon-alcoholic fatty liver diseaseNO, nitric oxideportal hypertensionPP, portal pressurePR, pulse rateSEM, scanning electron microscopyTBW, total body weightTEM, transmission electron microscopythromboxane A2transhepatic pressure gradientTxA2, thromboxane A2TXAS, thromboxane synthaseZFR, Zucker fatty rats

Identifiers

PMID35036886
PMCPMC8749167
OpenAlexW3217414126

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.