Evidence map›Paper›PMID 29492830›Full record

ReviewClinical journal of gastroenterology2018

The genetic backgrounds in nonalcoholic fatty liver disease.

Yuya Seko, Kanji Yamaguchi, Yoshito Itoh

Open access · bronzeAbstract readReview
PubMed Publisher
In one paragraph

Review in Clinical journal of gastroenterology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
5.3field-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

28 citing papers in PubMed, 54 citations in OpenAlex.

  1. Trial
  2. Article
  3. Genetic Predisposition to MASLD: Potential for Therapeutic Management.International journal of molecular sciences · 2026
    Review
  4. Mechanism and application ofFrontiers in cellular and infection microbiology · 2026
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Platelets in Non-alcoholic Fatty Liver Disease.Frontiers in pharmacology · 2022
    Review
  14. Review
  15. Observational
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article
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.

Yuya SekoMolecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto, 602-8566, Japan. yuyaseko@koto.kpu-m.ac.jp.
Kanji YamaguchiMolecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto, 602-8566, Japan.
Yoshito ItohMolecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto, 602-8566, Japan.
Kyoto Prefectural University of Medicine · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nonalcoholic fatty liver disease (NAFLD) is the most prevalent chronic liver disease worldwide. Nonalcoholic steatohepatitis (NASH), a severe form of NAFLD, can lead to hepatocellular carcinoma (HCC) and hepatic failure. The development and progression of NAFLD are determined by environmental and genetic factors. The effect of genetic factors has been demonstrated by familial studies, twin studies and several cross-sectional studies. In the past 10 years, genome-wide association studies have revealed several single nucleotide polymorphisms (SNPs) associated with the pathology of NAFLD. Among them, the Patatin-like phospholipase domain-containing 3 (PNPLA3) gene variant I148M showed a strong relationship with the development and progression of NAFLD, NASH, and NAFLD-related HCC. The transmembrane 6 superfamily member 2 (TM6SF2) gene variant E167 K was also associated with NAFLD, and it has a relationship with cardiovascular disease. Furthermore, several genes have been proposed as candidate genes to be associated with NAFLD based on case-control studies. We conducted a comprehensive literature search and review on the genetic background of NAFLD.

Indexed as

AcyltransferasesAdaptor Proteins, Signal TransducingDisease ProgressionGenetic BackgroundHumansLipaseMembrane ProteinsNon-alcoholic Fatty Liver DiseasePeroxisome Proliferator-Activated ReceptorsPhospholipases A2, Calcium-IndependentPhosphoric Diester HydrolasesPolymorphism, Single NucleotidePyrophosphatasesAcyltransferasesAdaptor Proteins, Signal Transducingectonucleotide pyrophosphatase phosphodiesterase 1GCKR protein, humanLipaseMembrane ProteinsPeroxisome Proliferator-Activated ReceptorsPhospholipases A2, Calcium-IndependentPhosphoric Diester HydrolasesPNPLA3 protein, humanPyrophosphatasesTM6SF2 protein, humanGenome-wide association study (GWAS)Glucokinase regulator (GCKR)Nonalcoholic fatty liver disease (NAFLD)PNPLA3TM6SF2

Identifiers

PMID29492830
OpenAlexW2793699024

What OpenQuestion holds

Textmetadata
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.