Evidence map›Paper›PMID 25163538›Full record

ArticleHepatology research : the official journal of the Japan Society of Hepatology2015

Inhibition of the CXCL12/CXCR4 chemokine axis with AMD3100, a CXCR4 small molecule inhibitor, worsens murine hepatic injury.

Yedidya Saiman, JingJing Jiao, M Isabel Fiel, Scott L Friedman, Costica Aloman, Meena B Bansal

Open access · greenAbstract read
In one paragraph

Article in Hepatology research : the official journal of the Japan Society of Hepatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

29 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
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  8. Recovered Hepatocytes Promote Macrophage Apoptosis Through CXCR4 After Acetaminophen-Induced Liver Injury in Mice.Toxicological sciences : an official journal of the Society of Toxicology · 2022
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  11. [Role of CXCL12-CXCR4/CXCR7 signal axis in liver regeneration and liver fibrosis].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2021
    Article
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  15. The liver fibrosis niche: Novel insights into the interplay between fibrosis-composing mesenchymal cells, immune cells, endothelial cells, and extracellular matrix.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2020
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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

6 authors at 1 institution in 1 country.

Yedidya SaimanDivision of Liver Diseases, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
JingJing JiaoDivision of Liver Diseases, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
M Isabel FielDivision of Liver Diseases, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Scott L FriedmanDivision of Liver Diseases, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Costica AlomanDivision of Liver Diseases, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Meena B BansalDivision of Liver Diseases, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Icahn School of Medicine at Mount Sinai · US

Funding

The Role of KLF6 in Hepatic FibrosisR01DK056621 · NIDDK · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI FRIEDMAN, SCOTT L. · 2000 to 2019
$6.2M
Autophagy during hepatic stellate cell activation in alcoholic liver injuryR01AA020709 · NIAAA · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI FRIEDMAN, SCOTT L. · 2011 to 2015
$1.8M
Modulation of liver fibrosis resolution by dendritic cellsK08DK088954 · NIDDK · UNIVERSITY OF ILLINOIS AT CHICAGO · PI ALOMAN, COSTICA · 2011 to 2015
$750k
IL-6 regulation of matrix degradation in liver fibrosisK08DK060474 · NIDDK · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI BANSAL, MEENA B · 2002 to 2006
$641k
Stellate cell-HIV interactions and Hepatic FibrosisR56DK092128 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI BANSAL, MEENA B · 2011 to 2011
$368k
Role of Matrix Metalloproteinase-2 in Liver FibrosisR03DK071745 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI BANSAL, MEENA B · 2006 to 2007
$167k
Biliary Epithelial Cell-derived SDF-1a in Hepatic Fibrogenesis and InflammationF30DK090986 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI SAIMAN, YEDIDYA · 2011 to 2014
$143k
NIAAA NIH HHS R01 AA020709NIDDK NIH HHS F30 DK090986NIDDK NIH HHS K08 DK060474NIDDK NIH HHS K08 DK088954NIDDK NIH HHS R01 DK056621NIDDK NIH HHS R03 DK071745NIDDK NIH HHS R56 DK092128
6 · The paper itself

Abstract

aimActivation of hepatic stellate cells and development of chronic inflammation are two key features in the progression of hepatic fibrosis. We have shown that in vitro activated stellate cells increase their expression of CXCL12 as well as the receptor CXCR4 and that receptor engagement promotes a profibrogenic phenotype. Furthermore, injury promotes increased hepatic expression of CXCL12 and a massive infiltration of CXCR4-expressing leukocytes, granulocytes and myeloid cells. The primary site of inflammatory cell accumulation is around the CXCL12-rich portal tracts and within fibrotic septae, indicating a role for CXCR4 during injury. In order to characterize the relevance of the CXCR4/CXCL12 chemokine axis during hepatic injury we inhibited the axis using AMD3100, a CXCR4 small molecule inhibitor, in models of chronic and acute liver injury.

methodsMice were subjected to acute and chronic CCl4 liver injury with and without AMD3100 administration. The degree of liver injury, fibrosis and the composition of the intrahepatic inflammatory response were characterized.

resultsTreatment of mice with AMD3100 in the chronic CCl4 model of liver injury led to an increase in hepatic inflammation and fibrosis with a specific increase in intrahepatic neutrophils. Furthermore, in an acute model of CCl4 -induced liver injury, AMD3100 led to an increase in the number of intrahepatic neutrophils and a trend towards worse necrosis.

conclusionTogether, this data suggests that inhibition of the CXCR4/CXCL12 chemokine axis is injurious through modulation of the hepatic inflammatory response and that this axis may serve a protective role in liver injury.

Indexed as

CXCL12CXCR4hepatic stellate cellsliver fibrosis

Identifiers

PMID25163538
PMCPMC4344928
OpenAlexW1951641979

What OpenQuestion holds

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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.