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A Method to Study the C924T Polymorphism of the Thromboxane A2 Receptor Gene
Published on: April 1, 2019
The Connexin37 gene C1019T polymorphism and risk of coronary artery disease: a meta-analysis
Zhijun Wu1, Yuqing Lou2, Wei Jin1
1Department of Cardiology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, PR China.
Insights
The Connexin37 C1019T polymorphism is not linked to coronary artery disease (CAD) risk overall. However, the 1019T allele is a moderate risk factor for myocardial infarction (MI), with diabetes mellitus potentially explaining study variations.
Area of Science:
- Genetics
- Cardiovascular Disease Epidemiology
- Molecular Biology
Background:
- The Connexin37 C1019T polymorphism is hypothesized to increase coronary artery disease (CAD) susceptibility.
- Previous studies on this association have produced conflicting results, necessitating further investigation.
Purpose of the Study:
- To conduct a comprehensive meta-analysis investigating the association between the Connexin37 C1019T polymorphism and the risk of coronary artery disease (CAD).
Main Methods:
- A meta-analysis was performed on 11 studies involving 5535 CAD patients and 5626 controls.
- Data were analyzed using a random-effects model to calculate odds ratios and confidence intervals.
- Publication bias was assessed using Egger's test, Begg-Mazemdar test, and funnel plots.
Main Results:
- The C1019T polymorphism was not significantly associated with overall CAD risk (p = 0.34).
- However, the 1019T allele showed a significant association with an increased risk of myocardial infarction (MI) (p < 0.001).
- Meta-regression suggested that varying proportions of diabetes mellitus (DM) across studies contributed significantly to heterogeneity (p = 0.014).
Conclusions:
- The Connexin37 C1019T polymorphism may represent a moderate risk factor specifically for myocardial infarction (MI).
- Diabetes mellitus (DM) is identified as a likely source of heterogeneity in studies examining this genetic polymorphism and cardiovascular disease risk.
Background And Aims:
Mounting data have emerged suggesting that the Connexin37 C1019T polymorphism increases susceptibility to coronary artery disease (CAD). However, previous studies yielded conflicting results. In the current study, a comprehensive meta-analysis was performed to investigate whether the C1019T polymorphism is associated with CAD risk.
Methods:
A total of 11 studies examining the C1019T polymorphism and CAD were identified using MEDLINE, Embase, CNKI, Wanfang and CBM, in which 5535 CAD patients and 5626 controls were analyzed. A random-effects model was used to calculate odd ratios and confidence intervals, while addressing between-study heterogeneity. Publication bias was weighed using the Egger's test, Begg-Mazemdar test and funnel plot.
Results:
In genetic models with striking heterogeneity, the risk of CAD was not associated with the C1019T polymorphism (allele comparison: p = 0.34, OR = 1.11, 95% CI 0.90-1.36). Stratification by disease endpoints indicated that the 1019T allele was significantly associated with myocardial infarction (MI) (allele comparison: p <0.001, OR = 1.59, 95% CI 1.24-2.03). Further meta-regression analysis indicated that a large proportion of heterogeneity was probably due to the varying proportions of diabetes mellitus (DM) across studies (p = 0.014).
Conclusions:
Our results indicated that the C1019T polymorphism may be a moderate risk factor for MI and that DM was likely a potential source of between-study heterogeneity.
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