Evidence map›Paper›PMID 28445509›Full record

ArticlePloS one2017

Functional genetic variants within the SIRT2 gene promoter in acute myocardial infarction.

Wentao Yang, Feng Gao, Pei Zhang, Shuchao Pang, Yinghua Cui, Lixin Liu, Guanghe Wei, Bo Yan

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. 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
1.2field-weighted citation impact, top 23% 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, 25 citations in OpenAlex.

  1. Pooled it
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  11. The role of SIRT2 in vascular-related and heart-related diseases: A review.Journal of cellular and molecular medicine · 2021
    Review
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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 3 institutions in 1 country.

Wentao YangDepartment of Medicine, Shandong University School of Medicine, Jinan, Shandong, China.
Feng GaoDepartment of Medicine, Shandong University School of Medicine, Jinan, Shandong, China.
Pei ZhangCollege of Clinical Medicine, Xinxiang Medical University, Xinxiang, Henan, China.
Shuchao PangShandong Provincial Key Laboratory of Cardiac Disease Diagnosis and Treatment, Affiliated Hospital of Jining Medical University, Jining Medical University, Jining, Shandong, China.
Yinghua CuiDivision of Cardiology, Affiliated Hospital of Jining Medical University, Jining Medical University, Jining, Shandong, China.
Lixin LiuDivision of Cardiology, Affiliated Hospital of Jining Medical University, Jining Medical University, Jining, Shandong, China.
Guanghe WeiDivision of Cardiology, Affiliated Hospital of Jining Medical University, Jining Medical University, Jining, Shandong, China.
Bo YanShandong Provincial Key Laboratory of Cardiac Disease Diagnosis and Treatment, Affiliated Hospital of Jining Medical University, Jining Medical University, Jining, Shandong, China.ORCID http://orcid.org/0000-0003-1391-5683
Affiliated Hospital of Jining Medical University · CNShandong University · CNXinxiang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Coronary artery disease (CAD), including acute myocardial infarction (AMI) is the complication of atherosclerosis. Recently, genome-wide association studies have identified a large number of CAD-related genetic variants. However, only 10% of CAD cases could be explained. Low frequent and rare genetic variants have been recently proposed to be main causes for CAD. SIRT2 is a member of sirtuin family, NAD(+)-dependent class III deacetylases. SIRT2 is involved in genomic stability, metabolism, inflammation, oxidative stress and autophagy, as well as in platelet function. Thus, we hypothesized that genetic variants in SIRT2 gene may contribute to AMI. In this study, SIRT2 gene promoter was analyzed in large cohorts of AMI patients (n = 375) and ethnic-matched controls (n = 377). Three novel heterozygous DSVs (g.38900888_91delTAAA, g.38900270A>G and g.38899853C>T) were identified in three AMI patients, but in none of controls. These DSVs significantly altered the transcriptional activity of the SIRT2 gene promoter (P<0.05) in both HEK-293 and H9c2 cells. Five novel heterozygous DSVS (g.38900562C>T, g.38900413A>C, g.38900030G>A, g.38899925A>C and g.38899852C>T) were only found in controls, which did not significantly affected SIRT2 gene promoter activity (P>0.05). In addition, four novel heterozygous DSVs and five SNPs were found in both AMI patients and control with similar frequencies (P>0.05), two SNPs of which were examined and did not affect SIRT2 gene promoter activity (P>0.05). Taken together, the DSVs identified in AMI patients may change SIRT2 level by affecting the transcriptional activity of SIRT2 gene promoter, contributing to the AMI development as a rare risk factor.

Indexed as

Genetic VariationAcute DiseaseAdultAgedAged, 80 and overAllelesCase-Control StudiesCell LineDNAFemaleGene FrequencyGenotypeHEK293 CellsHeterozygoteHumansMaleDNASIRT2 protein, humanSirtuin 2Transcription Factors

Identifiers

PMID28445509
PMCPMC5406008
OpenAlexW2609510962

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.