Association of MTHFR and DNMT-1 Gene Polymorphisms with Acute Coronary Syndrome in Patients Admitted to the Emergency Department

MTHFR 和 DNMT-1 基因多态性与急诊科收治患者急性冠脉综合征的相关性

阅读:2

Abstract

Background/Objectives: Acute coronary syndrome (ACS) is a critical cardiovascular condition influenced by genetic and environmental factors. Polymorphisms in methylenetetrahydrofolate reductase (MTHFR) and deoxyribonucleic acid methyltransferase-1 (DNMT-1) genes are linked to cardiovascular diseases, yet their specific roles in ACS pathogenesis remain unclear. This study examines the association of MTHFR C677T and DNMT-1 +32204 A/G polymorphisms with ACS and their potential contribution to genetic risk profiling. Methods: A case-control study was conducted with 212 participants, including 106 ACS patients and 106 controls. Peripheral blood samples were collected and analyzed to determine genotypic and allelic frequencies using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique. Statistical analyses were performed to assess associations between gene polymorphisms and ACS risk. Results: The MTHFR C677T polymorphism showed a strong association with ACS. The CC genotype significantly increased risk (OR: 7.34; 95% CI: 2.28-23.6; p < 0.001), while the C allele was also associated with higher susceptibility (OR: 2.21; 95% CI: 1.46-3.35; p < 0.001). Conversely, the T allele exhibited a protective effect, being more frequent in controls (62.9% vs. 37.1% in ACS; p = 0.000). Elevated troponin I levels in ACS patients with the TT genotype (p = 0.025) suggested a link between MTHFR variants and disease severity. However, DNMT-1 +32204 A/G polymorphisms showed no significant association with ACS risk. Conclusions: The MTHFR C677T polymorphism influences ACS susceptibility, with the CC genotype as a risk factor and the T allele offering potential protection.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。