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Background  ATP-binding cassette transporter A1 (ABCA1) plays a major role in high-density lipoprotein (HDL) metabolism and reverse cholesterol transport (RCT) and exerts anti-inflammatory effects. Increased  ABCA1  promoter methylation level may result in the progression of coronary artery disease. Thus, the present study investigated the association between promoter methylation status of  ABCA1  and inflammation in the development of premature coronary artery disease (pCAD).    Methods  PCAD patients and healthy individuals ( n  = 90 each) were recruited from the Characteristic Medical Center of the Chinese People's Armed Police Force from June to December 2019. Using pyrosequencing, the levels of  ABCA1  promoter methylation in their blood samples were evaluated. Serum concentrations of lipids, interleukin 1β (IL-1β), C-reactive protein (CRP), and circulating free DNA/Neutrophil extracellular traps (cfDNA/NETs) were also routinely measured and compared between the two groups.  P  values < 0.05 were considered statistically significant.    Results  The mean  ABCA1  promoter methylation levels were significantly higher in the pCAD group than in the control group (44.24% ± 3.66 vs. 36.05% ± 2.99,  P  < 0.001). Based on binary logistic regression analysis,  ABCA1  promoter methylation level was identified as an independent risk factor for pCAD development (odds ratio = 2.878, 95% confidence interval: 1.802–4.594,  P  < 0.001). Furthermore,  ABCA1  promoter methylation levels were negatively correlated with HDL levels ( r  =  − 0.488,  P  < 0.001) and positively correlated with the levels of CRP, cfDNA/NETs, and IL-1β ( r  = 0.389, 0.404, 0.385, respectively;  P  < 0.001). Multiple regression analysis showed that the serum levels of CRP, IL-1β, and cfDNA/NETs independently affect  ABCA1  promoter methylation.    Conclusions  Our findings indicate that high methylation levels at the  ABCA1  promoter are associated with low HDL cholesterol levels and an increased risk of pCAD. Inflammatory factors and NETs may be involved in the progression of pCAD by affecting  ABCA1  promoter methylation levels.

Effect of ABCA1 promoter methylation on premature coronary artery disease and its relationship with inflammation