Evidence map›Paper›PMID 32039405›Full record

ArticleJHEP reports : innovation in hepatology2020

A blocking monoclonal antibody to CCL24 alleviates liver fibrosis and inflammation in experimental models of liver damage.

Michal Segal-Salto, Neta Barashi, Avi Katav, Vicktoria Edelshtein, Arnon Aharon, Sharon Hashmueli, Jacob George, Yaakov Maor, Massimo Pinzani, Dan Haberman and 3 more

Open access · goldAbstract read
In one paragraph

Article in JHEP reports : innovation in hepatology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.5field-weighted citation impact, top 4% 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

38 citing papers in PubMed, 53 citations in OpenAlex.

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  20. Current Therapeutics in Primary Sclerosing Cholangitis.Journal of clinical and translational hepatology · 2023
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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

13 authors at 4 institutions in 3 countries.

Michal Segal-SaltoChemomAb, Tel Aviv, Israel.
Neta BarashiChemomAb, Tel Aviv, Israel.
Avi KatavChemomAb, Tel Aviv, Israel.
Vicktoria EdelshteinChemomAb, Tel Aviv, Israel.
Arnon AharonChemomAb, Tel Aviv, Israel.
Sharon HashmueliChemomAb, Tel Aviv, Israel.
Jacob GeorgeHeart Center, Kaplan Medical Center, Rehovot, Affiliated to the Hebrew University, Jerusalem, Israel.
Yaakov MaorInstitute of Gastroenterology and Hepatology, Kaplan Medical Center, Rehovot, Israel.
Massimo PinzaniUCL Institute for Liver and Digestive Health, University College of London, London, UK.
Dan HabermanHeart Center, Kaplan Medical Center, Rehovot, Affiliated to the Hebrew University, Jerusalem, Israel.
Andrew HallUCL Institute for Liver and Digestive Health, University College of London, London, UK.
Scott FriedmanDivision of Liver Diseases, Department of Medicine, Icahn School of Medicine at Mount Sinai, NY, USA.
Adi MorChemomAb, Tel Aviv, Israel.
Kaplan Medical Center · ILIcahn School of Medicine at Mount Sinai · USRoyal Free London NHS Foundation Trust · GBUniversity College London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND &

aimsC-C motif chemokine ligand 24 (CCL24) is a chemokine that regulates inflammatory and fibrotic activities through its receptor, C-C motif chemokine receptor (CCR3). The aim of the study was to evaluate the involvement of the CCL24-CCR3 axis in liver fibrosis and inflammation and to assess the potential of its blockade, by a monoclonal anti-CCL24 antibody, as a therapeutic strategy for non-alcoholic steatohepatitis (NASH) and liver fibrosis.

methodsExpression of CCL24 and CCR3 was evaluated in liver biopsies and blood samples. CCL24 involvement in NAFLD/NASH pathogenesis was assessed in

resultsPatients with NASH and advanced NAFLD exhibited significant expression of both CCL24 and CCR3 in liver and blood samples. In the experimental MCD-diet model,

conclusionOur results reveal that blocking CCL24 significantly attenuates liver fibrosis and inflammation and may have a potential therapeutic effect in patients with NASH and/or liver fibrosis. LAY SUMMARY: CCL24 is a chemokine that regulates inflammation and fibrosis. It was found to be significantly expressed in patients with non-alcoholic steatohepatitis, in whom it regulates profibrotic processes in the liver. Herein, we show that blockade of CCL24 using a monoclonal antibody robustly attenuated liver fibrosis and inflammation in animal models, thus suggesting a potential therapeutic role for an anti-CCL24 agent.

Indexed as

ALT, alanine aminotransferaseAntibodyAST, aspartate aminotransferaseCCL24CCL24, C-C motif chemokine ligand 24C-C motif chemokine ligand 24CCR3, C-C motif chemokine receptor 3CM-101FibrosisHSCs, hepatic stellate cellsIL-6, interleukin-6MCD, methionine-choline deficientMFI, median fluorescence intensityMMP, matrix metallopeptidaseNAFLD, non-alcoholic fatty liver diseaseNASH, non-alcoholic steatohepatitisNAS, NAFLD activity scoreNon-alcoholic fatty liver diseaseNon-alcoholic steatohepatitisPBMC, peripheral blood mononuclear cellsTAA, thioacetamideWT, wild-typeα-SMA, α-smooth muscle actin

Identifiers

PMID32039405
PMCPMC7005554
OpenAlexW2996908093

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.