Evidence map›Paper›PMID 27677852›Full record

ArticleScientific reports2016

Dimethylarginine Dimethylaminohydrolase 2 (DDAH 2) Gene Polymorphism, Asymmetric Dimethylarginine (ADMA) Concentrations, and Risk of Coronary Artery Disease: A Case-Control Study.

Chao Xuan, Long-Qiang Xu, Qing-Wu Tian, Hui Li, Qing Wang, Guo-Wei He, Li-Min Lun

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
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

14 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. The Emerging Role of the DDAH Proteins in Psychiatric Disorders.Biological psychiatry global open science · 2025
    Review
  3. Article
  4. Polymorphism (-499C/G) inArchives of endocrinology and metabolism · 2021
    Article
  5. Neural regeneration research · 2021
    Article
  6. Review
  7. Article
  8. The Functional Polymorphism ofFrontiers in cardiovascular medicine · 2021
    Article
  9. Review
  10. Article
  11. Review
  12. Observational
  13. Article
  14. 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

7 authors at 3 institutions in 2 countries.

Chao XuanDepartment of Clinical Laboratory, The Affiliated Hospital of Qingdao University, Qingdao, China.
Long-Qiang XuDepartment of Clinical Laboratory, The Affiliated Hospital of Qingdao University, Qingdao, China.
Qing-Wu TianDepartment of Clinical Laboratory, The Affiliated Hospital of Qingdao University, Qingdao, China.
Hui LiDepartment of Clinical Laboratory, The Affiliated Hospital of Qingdao University, Qingdao, China.
Qing WangDepartment of Clinical Laboratory, The Affiliated Hospital of Qingdao University, Qingdao, China.
Guo-Wei HeDepartment of Surgery, TEDA International Cardiovascular Hospital, Tianjin &The Affiliated Hospital of Hangzhou Normal University, Hangzhou, China.
Li-Min LunDepartment of Clinical Laboratory, The Affiliated Hospital of Qingdao University, Qingdao, China.
Affiliated Hospital of Qingdao University · CNQingdao University · CNAffiliated Hospital of Hangzhou Normal University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Asymmetric dimethylarginine (ADMA) has been shown to be an independent predictor of cardiovascular diseases. Dimethylarginine dimethylaminohydrolase 2 (DDAH 2) promotes the metabolism of ADMA and plays a key role in the regulation of acute inflammatory response. With the present study, we investigated the relationship between DDAH 2 polymorphisms and risk of coronary artery disease (CAD) and its association to plasma ADMA concentrations. We used the haplotype-tagging SNP approach to identify tag SNPs in DDAH 2. The SNPs were genotyped by PCR and sequenced in 385 CAD patients and 353 healthy controls. Plasma concentrations of ADMA were determined using enzyme-linked immunosorbent assay (ELISA). A promoter polymorphism -449C/G (rs805305) in DDAH 2 was identified. Compared with the ADMA concentrations in CC genotype (0.328 ± 0.077 μmol/l), ADMA concentrations in CG + GG genotype were significantly increased (0.517 ± 0.090 μmol/l, P < 0.001). No significant associations between the -449C/G and risk of CAD were detected in the genetic models. The results of this study suggest that Genetic -499C/G polymorphism in DDAH 2 gene may affect the plasma ADMA concentrations in patients with CAD. However, it does not indicate a novel genetic risk marker for CAD.

Identifiers

PMID27677852
PMCPMC5039408
OpenAlexW2525683644

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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.