Background/Aim: Decreased mitochondrial DNA copy number (mtDNA-CN) has been associated with coronary artery disease (CAD). We aimed to clarify the difference between stable CAD (SCAD) and acute coronary syndrome (ACS) regarding mtDNA-CN and the DNA methylation ratio in regions influencing the regulation of mitochondrial biogenesis. Materials and Methods: Using quantitative real-time polymerase chain reaction, mtDNA-CN was measured in peripheral blood leukocytes sampled from 50 patients with SCAD and 50 with ACS. We then conducted bisulfite modification of DNA followed by methylation-specific polymerase chain reaction to quantify mtDNA methylation in the mitochondrial D-loop region (mtDLR) and nuclear DNA methylation in the promoter region of nuclear peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PPARGC1A) gene. Results: Compared to patients with SCAD, those with ACS had significantly lower relative mtDNA-CN (0.89±0.24 vs. 1.00±0.28, p=0.013) and higher DNA methylation ratio of the mtDLR (1.11±0.24 vs. 1.00±0.25, p=0.027) Conclusion: Our findings suggest that increased DNA methylation in the mtDLR, which translates into reduced mtDNA content, may affect the clinical phenotype of CAD.

中文翻译：

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急性冠状动脉综合征的线粒体 DNA 甲基化高于稳定型冠状动脉疾病

背景/目的：减少的线粒体 DNA 拷贝数 (mtDNA-CN) 与冠状动脉疾病 (CAD) 相关。我们旨在阐明稳定型 CAD (SCAD) 和急性冠状动脉综合征 (ACS) 在 mtDNA-CN 和影响线粒体生物发生调节的区域中的 DNA 甲基化比率方面的差异。材料和方法：使用定量实时聚合酶链反应，在 50 名 SCAD 和 50 名 ACS 患者的外周血白细胞中测量 mtDNA-CN。然后我们对 DNA 进行亚硫酸氢盐修饰，然后进行甲基化特异性聚合酶链反应，以量化线粒体 D 环区域 (mtDLR) 中的 mtDNA 甲基化和核过氧化物酶体增殖物激活受体 γ 共激活因子 1-α 启动子区域中的核 DNA 甲基化。 PPARGC1A) 基因。结果：