Evidence map›Paper›PMID 24039859›Full record

ArticlePloS one2013

Hepatocellular proliferation correlates with inflammatory cell and cytokine changes in a murine model of nonalchoholic fatty liver disease.

Michael N Vansaun, Alisha M Mendonsa, D Lee Gorden

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 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

36 citing papers in PubMed, 58 citations in OpenAlex.

  1. Trial
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  8. Development of a hepatic cryoinjury model to study liver regeneration.bioRxiv : the preprint server for biology · 2024
    Article
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  11. Review
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  13. Liver Injury Increases the Incidence of HCC following AAV Gene Therapy in Mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2021
    Article
  14. Article
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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

3 authors at 1 institution in 1 country.

Michael N VansaunDepartment of Cancer Biology, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America ; Department of Surgery, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America.
Alisha M Mendonsa
D Lee Gorden
Vanderbilt University Medical Center · US

Funding

Molecular Determinants of Tumor Progression in A Steatolic Liver MicroenvironmentU01CA143072 · NCI · VANDERBILT UNIVERSITY · PI GORDEN, DAVID L, MOSES, HAROLD L · 2009 to 2013
$1.4M
NCI NIH HHS 5U01CA143072-03NCI NIH HHS U01 CA143072
6 · The paper itself

Abstract

Nonalchoholic fatty liver disease (NAFLD) is a problem of increasing prevalence and clinical significance worldwide and is associated with increased risk of development of end stage liver disease and cirrhosis, and can be complicated by hepatocellular carcinoma (HCC). NAFLD is characterized by physical and molecular changes in the liver microenvironment which include an influx of inflammatory cell populations, fibrosis, changes in gene expression, and cytokine production. To better understand changes to the liver in the setting of steatosis, we used a murine model of diet induced hepatic steatosis and corroborated our results with human patient samples of NAFLD. Among the cellular changes, we identified a significant increase in hepatocellular proliferation in the setting of steatosis as compared to controls. Analysis of inflammatory cell populations revealed increased infiltration of CD11b positive myeloid and CD3 positive lymphocytic cell populations in steatotic livers compared to normal livers. Resident Kupffer cells of the liver comprise the largest percentage of these myeloid cells and appear to be responsible for important cytokine alterations impacting proliferation of cells in the liver microenvironment. Significant alterations in cytokine profiles in the plasma and liver tissue lysates from normal and steatotic mice were detected including leptin, CXCL1, CXCL2, and CXCL16 that were further shown to directly increase hepatocyte proliferation in vitro. This increased hepatocellular proliferation and turnover in the setting of steatosis may play important roles in the progression and complications of NAFLD.

Indexed as

AnimalsCarcinoma, HepatocellularCell Line, TumorCell ProliferationCell Transformation, NeoplasticCytokinesDisease Models, AnimalFatty LiverHepatocytesHumansInflammationLiverLiver NeoplasmsLymphocytesMaleMiceCytokines

Identifiers

PMID24039859
PMCPMC3767686
OpenAlexW2077280576

What Socratic holds

Textmetadata
LicenceCC0
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 Socratic graph.