GST null polymorphisms may affect the risk of coronary artery disease: evidence from a meta-analysis
- PDF / 1,404,299 Bytes
- 10 Pages / 595.276 x 790.866 pts Page_size
- 73 Downloads / 154 Views
RESEARCH
Open Access
GST null polymorphisms may affect the risk of coronary artery disease: evidence from a meta-analysis Hongling Su*, Yunshan Cao, Jing Li, Yan Zhu and Xuming Ma
Abstract Background: Whether glutathione S-transferase (GST) null polymorphisms, namely GSTM1 null, GSTP1 null and GSTT1 null polymorphisms, influence the risk of coronary artery disease (CAD) or not remains unclear. Thus, the authors performed a meta-analysis to more robustly estimate associations between GST null polymorphisms and the risk of CAD by integrating the results of previous publications. Methods: Medline, Embase, Wanfang, VIP and CNKI were searched comprehensively for eligible studies, and 45 genetic association studies were finally selected to be included in this meta-analysis. Results: We found that GSTM1 null polymorphism was significantly associated with the risk of CAD in overall population (OR = 1.37, p = 0.003) and mixed population (OR = 1.61, p = 0.004), GSTP1 null polymorphism was significantly associated with the risk of CAD in overall population (OR = 1.23, p = 0.03), whereas GSTT1 null polymorphism was significantly associated with the risk of CAD in overall population (OR = 1.23, p = 0.02), Caucasians (OR = 1.23, p = 0.02) and East Asians (OR = 1.38, p < 0.0001). Conclusions: This meta-analysis demonstrated that GSTM1 null, GSTP1 null and GSTT1 null polymorphisms were all significantly associated with an increased risk of CAD. Keywords: Glutathione S-transferase (GST), Null polymorphisms, Coronary artery disease (CAD), Meta-analysis
Background Coronary artery disease (CAD) is featured by stenosis or even occlusion of coronary arteries, and their associated myocardial ischemia or infarction [1, 2]. The exact cause and pathogenesis of CAD are still nuclear despite extensive researches. Nevertheless, accumulating evidence supports that genetic factors play a crucial part in its development. First, family aggregation of CAD has been observed extensively, and past twin studies have demonstrated that the heredity grade of CHD can be as high as 50% [3, 4]. Second, numerous genetic polymorphisms have been found to be associated with an increased risk * Correspondence: [email protected] Department of Cardiology, Gansu Provincial People’s Hospital, No. 204 of Donggang West Road, Lanzhou 730000, Gansu, China
of CAD by previous genetic association studies, and screening of common causal mutations has also been demonstrated to be an efficient way to predict the individual risk of developing CAD [5, 6]. Overall, these findings jointly indicate that genetic architecture is important for the occurrence and development of CAD. Oxidative stress, characterized by accumulation of free radicals, membrane lipid peroxidation and DNA damage, has been found to play a critical role in the pathogenesis of various atherothrombotic disorders including CAD [7, 8]. Glutathione-S-transferases (GSTs) are a group of enzymes that play vital roles in regulating cellular detoxification of various exogenous toxins [9]. Moreover, it has been
Data Loading...
