Evidence map›Paper›PMID 32093693›Full record

ArticleLipids in health and disease2020

Independent and joint correlation of PNPLA3 I148M and TM6SF2 E167K variants with the risk of coronary heart disease in patients with non-alcoholic fatty liver disease.

Jian-Ting Wu, Shou-Sheng Liu, Xiang-Jun Xie, Qun Liu, Yong-Ning Xin, Shi-Ying Xuan

Open access · goldAbstract read
In one paragraph

Article in Lipids in health and disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 9% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. The Human PNPLA3FASEB bioAdvances · 2026
    Article
  4. Article
  5. Review
  6. International journal of molecular sciences · 2025
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Mechanisms Behind NAFLD: a System Genetics Perspective.Current atherosclerosis reports · 2023
    Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. 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

6 authors at 1 institution in 1 country.

Jian-Ting WuDepartment of Gastroenterology, Qingdao Municipal Hospital, Qingdao University, Qingdao, 266011, China.
Shou-Sheng LiuCentral Laboratories, Qingdao Municipal Hospital, Qingdao University, Qingdao, 266071, China.
Xiang-Jun XieDepartment of Gastroenterology, Qingdao Municipal Hospital, Qingdao University, Qingdao, 266011, China.
Qun LiuDepartment of Gastroenterology, Qingdao Municipal Hospital, Qingdao University, Qingdao, 266011, China.
Yong-Ning XinDigestive Disease Key Laboratory of Qingdao, Qingdao, 266071, China. xinyongning@163.com.ORCID http://orcid.org/0000-0002-3692-7655
Shi-Ying XuanDepartment of Gastroenterology, Qingdao Municipal Hospital, Qingdao University, Qingdao, 266011, China. xuansydxy@163.com.
Qingdao University · CN

Funding

National Natural Science Foundation of China 31770837Qingdao People's Livelihood Science and technology plan 18-6-1-68-nsh
6 · The paper itself

Abstract

backgroundCHD is reported to be the primary cause of death in patients with NAFLD. Genetic susceptibility genes contribute to the developmental risk of NAFLD or CHD. Whether the genetic factors could affect the risk of CHD in NAFLD patients is not clear. The aim of this study was to investigate the association of PNPLA3 I148M and TM6SF2 E167K variants with the risk of CHD in NAFLD patients in Chinese Han population. PATIENTS AND

methodsPNPLA3 I148M and TM6SF2 E167K variants were genotyped in a cohort of 189 patients with NAFLD and CHD, as well as 242 patients with NAFLD and 242 healthy controls by gene sequencing. Additionally, serum lipids profiles were determined by standard clinical laboratory methods.

resultsThe minor allele frequency of PNPLA3 I148M and TM6SF2 E167K were 0.39 and 0.06 in this cohort, respectively. The distributions of PNPLA3 I148M genotypes and alleles were significant different in NAFLD group vs controls and in NAFLD+CHD group vs NAFLD group (all P <  0.05). NAFLD patients who carry the CG + GG genotype suffered the relative lower risk of CHD than CC genotype carriers (OR = 0.6, 95%CI: 0.40-0.90, P = 0.01). In addition, PNPLA3 I148M and TM6SF2 E167K possess the joint correlation with the decreased risk of CHD in NAFLD patients with the increased number of risk alleles. Besides, PNPLA3 I148M and TM6SF2 E167K variants associated with the decreased serum lipid levels in overall series.

conclusionsThere was a joint protective correlation of PNPLA3 I148M and TM6SF2 E167K variants with the developmental risk of CHD in NAFLD patients. PNPLA3 I148M and TM6SF2 E167K variants might correlated with the decreased risk of CHD in NAFLD patients by associated with the reduced serum lipid levels.

Indexed as

AcyltransferasesAllelesCoronary DiseaseFemaleGene FrequencyGenetic Predisposition to DiseaseGenotypeHumansLipaseMaleMembrane ProteinsMiddle AgedNon-alcoholic Fatty Liver DiseasePhospholipases A2, Calcium-IndependentPolymorphism, Single NucleotideAcyltransferasesLipaseMembrane ProteinsPhospholipases A2, Calcium-IndependentPNPLA3 protein, humanTM6SF2 protein, humanCoronary heart diseaseNon-alcoholic fatty liver diseasePNPLA3 I148MTM6SF2 E167K

Identifiers

PMID32093693
PMCPMC7041191
OpenAlexW3010937035

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.