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.