Association between myeloperoxidase rs2333227 polymorphism and susceptibility to coronary heart disease

Abstract

Coronary heart disease (CHD) accounts for the most morbidity and mortality all over the world [1]. Heritable factors account for 30-60% of the susceptibility to coronary heart disease, and therefore genotypic variants are potential modifiers of predisposition to coronary heart disease. Our previous study demonstrated that apolipoprotein A1 polymorphism was associated with coronary artery disease [2]. Recently, researchers have revealed myeloperoxidase (MPO) as a new potential mutation associated with the pathogenesis of CHD [3]. In Piedrafita et al.'s study, MPO rs2333227 was reported to be associated with significantly decreased transcriptional activity due to the disruption of an SP1 (specificity protein-1)-binding site in an Alu hormone-responsive element [4]. To date, there have been many researchers studying the association between MPO rs2333227 and coronary heart disease. But the results were not consistent. Given the conflicting evidence on this issue, we conducted the present meta-analysis of all available studies to evaluate the association between MPO rs2333227 genetic polymorphism and the risk of coronary heart disease.We performed our meta-analysis according to the "Meta-analysis Of Observational Studies in Epidemiology" (MOOSE) proposal [5]. To identify eligible studies for this meta-analysis, two investigators (Yi-Qing Zhang and Yu-Feng Jiang) searched the PubMed, Web of Science, Embase, CNKI (Chinese National Knowledge Infrastructure) and WanFang database in all languages up to March 31, 2017, combined with a manual search of reference lists from identified studies. For the article search, the following combination of medical subject heading or suitable key words was used: coronary heart disease, coronary artery disease, ische mic heart disease, angina or myocardial infarction and myeloperoxidase rs2333227 and polymorphism. The inclusion criteria were preestablished: 1) case-control designed studies; 2) studies that evaluated the association of myeloperoxidase polymorphism and susceptibility to CHD; 3) provided detailed information on genotype frequency and 4) studies that provided sufficient data to calculate odds ratios (ORs) and 95% confidential intervals for extraction. Useful data in all eligible studies were extracted by two authors (Yi-Qing Zhang and Yu-Feng Jiang). Conflicts were discussed with a third investigator (Ya-Feng Zhou). Study quality was assessed according to the 9-point Newcastle-Ottawa Scale (NOS) [6]. We performed Hardy-Weinberg equilibrium (HWE) tests

Effects of E-Waste Exposure on Biomarkers of Coronary Heart Disease (CHD) and their Associations with Level of Heavy Metals in Blood

“…When the body is stimulated by external stimulation, the imbalance of OS result in the formation of signi cant amounts of lipid products and oxides in the arterial walls, which induces an immune response and an in ammatory reaction(Abraham and Marchuk 2014). Several studies have shown that MPO mediates the formation of OS and in ammatory reactions and is a signi cant in ammatory marker(Love et al 2017;Zhang et al 2020). Moreover, the oxidative modi cation of MPO causes the formation of arterial plaques, and the level of MPO is closely associated with CHD(Gorudko et al 2012).…”