Evidence map›Paper›PMID 33160101›Full record

ReviewMolecular metabolism2021

Genetic and epigenetic factors determining NAFLD risk.

Wenke Jonas, Annette Schürmann

Open access · goldAbstract readReview
In one paragraph

Review in Molecular metabolism, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
105citing papers in PubMed, 1 pooled it
10.6field-weighted citation impact, top 1% 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

105 citing papers in PubMed, 1 synthesis or guideline pooled it, 148 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Nutrients · 2024
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  14. The menopause-obesity axis in MASH progression: from estrogen decline to liver fibrosis.Frontiers in gastroenterology (Lausanne, Switzerland) · 2026
    Review
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45 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

2 authors at 2 institutions in 1 country.

Wenke JonasDepartment of Experimental Diabetology, German Institute of Human Nutrition Potsdam-Rehbruecke, Arthur-Scheunert-Allee 114-116, D-14558, Nuthetal, Germany; German Center for Diabetes Research (DZD), Ingolstädter Landstraße 1, D-85764, München-Neuherberg, Germany.
Annette SchürmannDepartment of Experimental Diabetology, German Institute of Human Nutrition Potsdam-Rehbruecke, Arthur-Scheunert-Allee 114-116, D-14558, Nuthetal, Germany; German Center for Diabetes Research (DZD), Ingolstädter Landstraße 1, D-85764, München-Neuherberg, Germany; University of Potsdam, Institute of Nutritional Sciences, Arthur-Scheunert-Allee 114-116, D-14558, Nuthetal, Germany; Faculty of Health Sciences, Joint Faculty of the Brandenburg University of Technology, Cottbus-Senftenberg, The Brandenburg Medical School Theodor Fontane and the University of Potsdam, Potsdam, Germany. Electronic address: schuermann@dife.de.
Deutsches Diabetes-Zentrum e.V. · DEUniversity of Potsdam · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHepatic steatosis is a common chronic liver disease that can progress into more severe stages of NAFLD or promote the development of life-threatening secondary diseases for some of those affected. These include the liver itself (nonalcoholic steatohepatitis or NASH; fibrosis and cirrhosis, and hepatocellular carcinoma) or other organs such as the vessels and the heart (cardiovascular disease) or the islets of Langerhans (type 2 diabetes). In addition to elevated caloric intake and a sedentary lifestyle, genetic and epigenetic predisposition contribute to the development of NAFLD and the secondary diseases. SCOPE OF REVIEW: We present data from genome-wide association studies (GWAS) and functional studies in rodents which describe polymorphisms identified in genes relevant for the disease as well as changes caused by altered DNA methylation and gene regulation via specific miRNAs. The review also provides information on the current status of the use of genetic and epigenetic factors as risk markers. MAJOR

conclusionWith our overview we provide an insight into the genetic and epigenetic landscape of NAFLD and argue about the applicability of currently defined risk scores for risk stratification and conclude that further efforts are needed to make the scores more usable and meaningful.

Indexed as

Epigenesis, GeneticGenetic Predisposition to DiseaseAnimalsCarcinoma, HepatocellularDiabetes Mellitus, Type 2Disease Models, AnimalDNA MethylationGene Expression RegulationGenome-Wide Association StudyHumansLiver CirrhosisLiver NeoplasmsMicroRNAsNon-alcoholic Fatty Liver DiseasePolymorphism, Single NucleotideRisk FactorsMicroRNAsEpigeneticsGenetic variantsNAFLDRisk score

Identifiers

PMID33160101
PMCPMC8324682
OpenAlexW3095035989

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.