Evidence map›Paper›PMID 25347188›Full record

ArticlePloS one2014

Comparative analysis and modeling of the severity of steatohepatitis in DDC-treated mouse strains.

Vikash Pandey, Marc Sultan, Karl Kashofer, Meryem Ralser, Vyacheslav Amstislavskiy, Julia Starmann, Ingrid Osprian, Christina Grimm, Hendrik Hache, Marie-Laure Yaspo and 6 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.2field-weighted citation impact, top 41% 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

7 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
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  5. Targeting the eicosanoid pathway in hepatocellular carcinoma.American journal of cancer research · 2021
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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

16 authors at 6 institutions in 2 countries.

Vikash PandeyMax Planck Institute for Molecular Genetics, Department Vertebrate Genomics, Berlin, Germany.
Marc SultanMax Planck Institute for Molecular Genetics, Department Vertebrate Genomics, Berlin, Germany.
Karl KashoferInstitute of Pathology, Medical University of Graz, Graz, Austria.
Meryem RalserMax Planck Institute for Molecular Genetics, Department Vertebrate Genomics, Berlin, Germany.
Vyacheslav AmstislavskiyMax Planck Institute for Molecular Genetics, Department Vertebrate Genomics, Berlin, Germany.
Julia StarmannGerman Cancer Research Center, Heidelberg, Germany.
Ingrid OsprianBIOCRATES Life Sciences AG, Innsbruck, Austria; LKH Wagna, Department of Internal Medicine, Wagna, Austria.
Christina GrimmRheumatology and Clinical Immunology, Charité-University Medicine, Berlin, Germany.
Hendrik HacheMax Planck Institute for Molecular Genetics, Department Vertebrate Genomics, Berlin, Germany.
Marie-Laure YaspoMax Planck Institute for Molecular Genetics, Department Vertebrate Genomics, Berlin, Germany; Dahlem Centre for Genome Research and Medical Systems Biology, Berlin, Germany.
Holger SültmannGerman Cancer Research Center, Heidelberg, Germany.
Michael TraunerHans Popper Laboratory of Molecular Hepatology, Division of Gastroenterology and Hepatology, Department of Medicine, Medical University of Vienna, Vienna, Austria.
Helmut DenkInstitute of Pathology, Medical University of Graz, Graz, Austria.
Kurt ZatloukalInstitute of Pathology, Medical University of Graz, Graz, Austria.
Hans LehrachMax Planck Institute for Molecular Genetics, Department Vertebrate Genomics, Berlin, Germany; Dahlem Centre for Genome Research and Medical Systems Biology, Berlin, Germany.
Christoph WierlingMax Planck Institute for Molecular Genetics, Department Vertebrate Genomics, Berlin, Germany.
Max Planck Institute for Molecular Genetics · DEMedical University of Graz · ATGerman Cancer Research Center · DEBiocrates Life Sciences (Austria) · ATCharité - Universitätsmedizin Berlin · DEMedical University of Vienna · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNon-alcoholic fatty liver disease (NAFLD) has a broad spectrum of disease states ranging from mild steatosis characterized by an abnormal retention of lipids within liver cells to steatohepatitis (NASH) showing fat accumulation, inflammation, ballooning and degradation of hepatocytes, and fibrosis. Ultimately, steatohepatitis can result in liver cirrhosis and hepatocellular carcinoma. METHODOLOGY AND

resultsIn this study we have analyzed three different mouse strains, A/J, C57BL/6J, and PWD/PhJ, that show different degrees of steatohepatitis when administered a 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) containing diet. RNA-Seq gene expression analysis, protein analysis and metabolic profiling were applied to identify differentially expressed genes/proteins and perturbed metabolite levels of mouse liver samples upon DDC-treatment. Pathway analysis revealed alteration of arachidonic acid (AA) and S-adenosylmethionine (SAMe) metabolism upon other pathways. To understand metabolic changes of arachidonic acid metabolism in the light of disease expression profiles a kinetic model of this pathway was developed and optimized according to metabolite levels. Subsequently, the model was used to study in silico effects of potential drug targets for steatohepatitis.

conclusionsWe identified AA/eicosanoid metabolism as highly perturbed in DDC-induced mice using a combination of an experimental and in silico approach. Our analysis of the AA/eicosanoid metabolic pathway suggests that 5-hydroxyeicosatetraenoic acid (5-HETE), 15-hydroxyeicosatetraenoic acid (15-HETE) and prostaglandin D2 (PGD2) are perturbed in DDC mice. We further demonstrate that a dynamic model can be used for qualitative prediction of metabolic changes based on transcriptomics data in a disease-related context. Furthermore, SAMe metabolism was identified as being perturbed due to DDC treatment. Several genes as well as some metabolites of this module show differences between A/J and C57BL/6J on the one hand and PWD/PhJ on the other.

Indexed as

AnimalsCluster AnalysisDisease Models, AnimalFatty LiverGene Expression ProfilingGene Expression RegulationMetabolic Networks and PathwaysMetabolomeMetabolomicsMiceNon-alcoholic Fatty Liver DiseasePhenotypeProteomicsPyridinesSeverity of Illness IndexSignal Transduction3,5-diethoxycarbonyl-1,4-dihydrocollidinePyridines

Identifiers

PMID25347188
PMCPMC4210132
OpenAlexW2013236381

What OpenQuestion holds

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LicenceCC BY
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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.