Evidence map›Paper›PMID 27308945›Full record

ArticleStem cells and development2016

Modeling Nonalcoholic Fatty Liver Disease with Human Pluripotent Stem Cell-Derived Immature Hepatocyte-Like Cells Reveals Activation of PLIN2 and Confirms Regulatory Functions of Peroxisome Proliferator-Activated Receptor Alpha.

Nina Graffmann, Sarah Ring, Marie-Ann Kawala, Wasco Wruck, Audrey Ncube, Hans-Ingo Trompeter, James Adjaye

Open access · hybridAbstract read
In one paragraph

Article in Stem cells and development, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
7.2field-weighted citation impact, top 3% 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

64 citing papers in PubMed, 117 citations in OpenAlex.

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4 more citing papers are in PubMed but not listed here.

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

7 authors at 1 institution in 1 country.

Nina Graffmann1 Institute for Stem Cell Research and Regenerative Medicine, Heinrich Heine University Düsseldorf , Düsseldorf, Germany .
Sarah Ring1 Institute for Stem Cell Research and Regenerative Medicine, Heinrich Heine University Düsseldorf , Düsseldorf, Germany .
Marie-Ann Kawala1 Institute for Stem Cell Research and Regenerative Medicine, Heinrich Heine University Düsseldorf , Düsseldorf, Germany .
Wasco Wruck1 Institute for Stem Cell Research and Regenerative Medicine, Heinrich Heine University Düsseldorf , Düsseldorf, Germany .
Audrey Ncube1 Institute for Stem Cell Research and Regenerative Medicine, Heinrich Heine University Düsseldorf , Düsseldorf, Germany .
Hans-Ingo Trompeter2 Institute for Transplantation Diagnostics and Cell Therapeutics, Heinrich Heine University Düsseldorf , Düsseldorf, Germany .
James Adjaye1 Institute for Stem Cell Research and Regenerative Medicine, Heinrich Heine University Düsseldorf , Düsseldorf, Germany .
Heinrich Heine University Düsseldorf · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nonalcoholic fatty liver disease (NAFLD/steatosis) is a metabolic disease characterized by the incorporation of fat into hepatocytes. In this study, we developed an in vitro model for NAFLD based on hepatocyte-like cells (HLCs) differentiated from human pluripotent stem cells. We induced fat storage in these HLCs and detected major expression changes of metabolism-associated genes, as well as an overall reduction of liver-related microRNAs. We observed an upregulation of the lipid droplet coating protein Perilipin 2 (PLIN2), as well as of numerous genes of the peroxisome proliferator-activated receptor (PPAR) pathway, which constitutes a regulatory hub for metabolic processes. Interference with PLIN2 and PPARα resulted in major alterations in gene expression, especially affecting lipid, glucose, and purine metabolism. Our model recapitulates many metabolic changes that are characteristic for NAFLD. It permits the dissection of disease-promoting molecular pathways and allows us to investigate the influences of distinct genetic backgrounds on disease progression.

Indexed as

Cell DifferentiationModels, BiologicalGene Expression ProfilingGene Knockdown TechniquesHepatocytesHep G2 CellsHumansLipid DropletsLipid MetabolismMicroRNAsNon-alcoholic Fatty Liver DiseaseOrgan SpecificityPerilipin-2Pluripotent Stem CellsPPAR alphaRNA, Small InterferingMicroRNAsPerilipin-2PPAR alphaRNA, Small Interfering

Identifiers

PMID27308945
PMCPMC4971413
OpenAlexW2482436688

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.