Evidence map›Paper›PMID 29222421›Full record

ArticleScientific reports2017

The Transcriptomic Signature Of Disease Development And Progression Of Nonalcoholic Fatty Liver Disease.

Sophie Cazanave, Alexei Podtelezhnikov, Kristian Jensen, Mulugeta Seneshaw, Divya P Kumar, Hae-Ki Min, Prasanna K Santhekadur, Bubu Banini, Adolfo Gabriele Mauro, Abdul M Oseini and 7 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
4.8field-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

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors at 3 institutions in 2 countries.

Sophie CazanaveDivision of Gastroenterology, Hepatology and Nutrition, Department of Internal Medicine, Virginia Commonwealth University, Richmond, VA, USA. sccncazanave@gmail.com.
Alexei PodtelezhnikovMerck Research Laboratories, Kenilworth, NJ, USA.
Kristian JensenMerck Research Laboratories, Kenilworth, NJ, USA.
Mulugeta SeneshawDivision of Gastroenterology, Hepatology and Nutrition, Department of Internal Medicine, Virginia Commonwealth University, Richmond, VA, USA.
Divya P KumarDivision of Gastroenterology, Hepatology and Nutrition, Department of Internal Medicine, Virginia Commonwealth University, Richmond, VA, USA.
Hae-Ki MinDivision of Gastroenterology, Hepatology and Nutrition, Department of Internal Medicine, Virginia Commonwealth University, Richmond, VA, USA.
Prasanna K SanthekadurDivision of Gastroenterology, Hepatology and Nutrition, Department of Internal Medicine, Virginia Commonwealth University, Richmond, VA, USA.
Bubu BaniniDivision of Gastroenterology, Hepatology and Nutrition, Department of Internal Medicine, Virginia Commonwealth University, Richmond, VA, USA.
Adolfo Gabriele MauroVCU Pauley Heart Center, Virginia Commonwealth University, Richmond, VA, USA.
Abdul M OseiniDivision of Gastroenterology, Hepatology and Nutrition, Department of Internal Medicine, Virginia Commonwealth University, Richmond, VA, USA.
Robert VincentDivision of Gastroenterology, Hepatology and Nutrition, Department of Internal Medicine, Virginia Commonwealth University, Richmond, VA, USA.
Keith Q TanisMerck Research Laboratories, Kenilworth, NJ, USA.
Andrea L WebberMerck Research Laboratories, Kenilworth, NJ, USA.
Liangsu WangMerck Research Laboratories, Kenilworth, NJ, USA.
Pierre BedossaDepartment of Pathology, Hospital Beaujon, University Paris-Diderot, Paris, France.
Faridoddin MirshahiDivision of Gastroenterology, Hepatology and Nutrition, Department of Internal Medicine, Virginia Commonwealth University, Richmond, VA, USA.
Arun J SanyalDivision of Gastroenterology, Hepatology and Nutrition, Department of Internal Medicine, Virginia Commonwealth University, Richmond, VA, USA. arun.sanyal@vcuhealth.org.
Virginia Commonwealth University · USMerck & Co., Inc., Rahway, NJ, USA (United States) · USDélégation Paris 7 · FR

Funding

Training Grant in Digestive Diseases and Liver DiseasesT32DK007150 · NIDDK · VIRGINIA COMMONWEALTH UNIVERSITY · PI SANYAL, ARUN J · 1986 to 2017
$4.2M
Molecular Determinants of Disease Progression in Nonalcoholic SteatohepatitisR01DK081410 · NIDDK · VIRGINIA COMMONWEALTH UNIVERSITY · PI SANYAL, ARUN J · 2009 to 2013
$1.7M
MicroRNA in Liver DevelopmentR03DK081450 · NIDDK · CHILDREN'S HOSP OF PHILADELPHIA · PI FRIEDMAN, JOSHUA R. · 2008 to 2009
$165k
NIDDK NIH HHS R01 DK081410NIDDK NIH HHS R03 DK081450NIDDK NIH HHS T32 DK007150
6 · The paper itself

Abstract

A longitudinal molecular model of the development and progression of nonalcoholic fatty liver disease (NAFLD) over time is lacking. We have recently validated a high fat/sugar water-induced animal (an isogenic strain of C57BL/6 J:129S1/SvImJ mice) model of NAFLD that closely mimics most aspects of human disease. The hepatic transcriptome of such mice with fatty liver (8 weeks), steatohepatitis with early fibrosis (16-24 weeks) and advanced fibrosis (52 weeks) after initiation of the diet was evaluated and compared to mice on chow diet. Fatty liver development was associated with transcriptional activation of lipogenesis, FXR-RXR, PPAR-α mediated lipid oxidation and oxidative stress pathways. With progression to steatohepatitis, metabolic pathway activation persisted with additional activation of IL-1/inhibition of RXR, granulocyte diapedesis/adhesion, Fc macrophage activation, prothrombin activation and hepatic stellate cell activation. Progression to advanced fibrosis was associated with dampening of metabolic, oxidative stress and cell stress related pathway activation but with further Fc macrophage activation, cell death and turnover and activation of cancer-related networks. The molecular progression of NAFLD involves a metabolic perturbation which triggers subsequent cell stress and inflammation driving cell death and turnover. Over time, inflammation and fibrogenic pathways become dominant while in advanced disease an inflammatory-oncogenic profile dominates.

Indexed as

Disease ProgressionGene Expression ProfilingAnimalsLiver CirrhosisMaleMiceMice, Inbred C57BLNon-alcoholic Fatty Liver DiseaseSignal Transduction

Identifiers

PMID29222421
PMCPMC5722878
OpenAlexW2771222944

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.