Evidence map›Paper›PMID 27494404›Full record

ArticlePloS one2016

HDAC9 Variant Rs2107595 Modifies Susceptibility to Coronary Artery Disease and the Severity of Coronary Atherosclerosis in a Chinese Han Population.

Xue-Bin Wang, Ya-di Han, Shrestha Sabina, Ning-Hua Cui, Shuai Zhang, Ze-Jin Liu, Cong Li, Fang Zheng

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. 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
1.7field-weighted citation impact, top 15% 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. Genetic Insights Into Coronary Microvascular Disease.Microcirculation (New York, N.Y. : 1994) · 2025
    Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  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

8 authors at 4 institutions in 1 country.

Xue-Bin WangCenter for Gene Diagnosis, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, China.
Ya-di HanCenter for Gene Diagnosis, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, China.
Shrestha SabinaCenter for Gene Diagnosis, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, China.
Ning-Hua CuiDepartment of Clinical Laboratory, Children's Hospital of Zhengzhou, Zhengzhou, Henan, China.
Shuai ZhangCenter for Gene Diagnosis, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, China.
Ze-Jin LiuCenter of Clinical Laboratory, Wuhan Asia Heart Hospital, Wuhan, Hubei, China.
Cong LiZhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Fang ZhengCenter for Gene Diagnosis, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, China.
Zhongnan Hospital of Wuhan University · CNWuhan University · CNSun Yat-sen University · CNZhengzhou Children's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A previous genome-wide association study showed that a single nucleotide polymorphism (SNP) rs2107595 in histone deacetylase 9 (HDAC9) gene was associated with large artery stroke (LAS) in Caucasians. Based on the similar atherosclerotic pathogenesis between LAS and coronary artery disease (CAD), we aimed to evaluate the associations of SNP rs2107595 with CAD risk and the severity of coronary atherosclerosis in a Chinese Han population, and explore the potential gene-environment interactions among SNP rs2107595 and conventional CAD risk factors. In a two-stage case-control study with a total of 2317 CAD patients and 2404 controls, the AG + AA genotypes of SNP rs2107595 were significantly associated with increased CAD risk (Adjusted odds ratio (OR) = 1.23, Padj = 0.001) and higher modified Gensini scores (Adjusted OR = 1.38, Padj < 0.001). These associations remained significant in subtype analyses for unstable angina pectoris (UAP), non-ST-segment elevation myocardial infarction (NSTEMI) and ST-segment elevation myocardial infarction (STEMI). Subgroup and multifactor dimensionality reduction analyses (MDR) further found the gene-environment interactions among SNP rs2107595, body mass index, type 2 diabetes and hyperlipidemia in CAD risk and the severity of coronary atherosclerosis. Moreover, patients with CAD had higher levels of HDAC9 mRNA expression and plasma HDAC9 than controls. Subsequent genotype-phenotype analyses observed the significant correlations of SNP rs2107595 with HDAC9 mRNA expression and plasma HDAC9 levels in controls and patients with NSTEMI and STEMI. Taken together, our data suggest that SNP rs2107595 may contribute to coronary atherosclerosis and CAD risk through a possible mechanism of regulating HDAC9 expression and gene-environment interactions.

Indexed as

Polymorphism, Single NucleotideAllelesAsian PeopleCase-Control StudiesChinaCoronary Artery DiseaseDiabetes Mellitus, Type 2Gene-Environment InteractionGenetic Predisposition to DiseaseHistone DeacetylasesHumansMyocardial InfarctionRepressor ProteinsHDAC9 protein, humanHistone DeacetylasesRepressor Proteins

Identifiers

PMID27494404
PMCPMC4975504
OpenAlexW2493856848

What OpenQuestion 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 OpenQuestion graph.