Evidence map›Paper›PMID 23799074›Full record

ArticlePloS one2013

The chemokine CCL3 promotes experimental liver fibrosis in mice.

Daniel Heinrichs, Marie-Luise Berres, Andreas Nellen, Petra Fischer, David Scholten, Christian Trautwein, Hermann E Wasmuth, Hacer Sahin

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

42 citing papers in PubMed, 72 citations in OpenAlex.

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  11. Hepatic inflammatory responses in liver fibrosis.Nature reviews. Gastroenterology & hepatology · 2023
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  19. Osr1 regulates hepatic inflammation and cell survival in the progression of non-alcoholic fatty liver disease.Laboratory investigation; a journal of technical methods and pathology · 2021
    Article
  20. 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

8 authors at 1 institution in 1 country.

Daniel HeinrichsMedical Department III, University Hospital Aachen, Aachen, Germany.
Marie-Luise Berres
Andreas Nellen
Petra Fischer
David Scholten
Christian Trautwein
Hermann E Wasmuth
Hacer Sahin
Universitätsklinikum Aachen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Liver fibrosis is associated with infiltrating immune cells and activation of hepatic stellate cells. We here aimed to investigate the effects of the CC chemokine CCL3, also known as macrophage inflammatory protein-1α, in two different fibrosis models. To this end, we treated mice either with carbon tetrachloride or with a methionine- and choline-deficient diet to induce fibrosis in CCL3 deficient and wild-type mice. The results show that the protein expression of CCL3 is increased in wild-type mice after chronic liver injury. Deletion of CCL3 exhibited reduced liver fibrosis compared to their wild-type counterparts. We could validate these results by treating the two mouse groups with either carbon tetrachloride or by feeding a methionine- and choline-deficient diet. In these models, lack of CCL3 is functionally associated with reduced stellate cell activation and liver immune cell infiltration. In vitro, we show that CCL3 leads to increased proliferation and migration of hepatic stellate cells. In conclusion, our results define the chemokine CCL3 as a mediator of experimental liver fibrosis. Thus, therapeutic modulation of CCL3 might be a promising target for chronic liver diseases.

Indexed as

AnimalsCarbon TetrachlorideCell ProliferationChemokine CCL3Enzyme-Linked Immunosorbent AssayLipogenesisLiver CirrhosisMaleMiceMice, Inbred BALB CMice, KnockoutT-LymphocytesCarbon TetrachlorideCcl3 protein, mouseChemokine CCL3

Identifiers

PMID23799074
PMCPMC3684603
OpenAlexW2093577520

What OpenQuestion holds

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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.