Association between DNA methylation and coronary heart disease or other atherosclerotic events: A systematic review

Abstract

Global DNA methylation seems to be not associated with CHD. The evidence from candidate-gene studies was limited. The EWAS identified a set of 84 genes highlighting the relevance of obesity, inflammation, lipid and carbohydrate metabolism in CHD. This set of genes could be prioritized in future studies assessing the role of DNA methylation in CHD.

Coronary artery disease in a rural population of Bangladesh: is dyslipidemia or adiposity a significant risk?

“…Additionally, it would have been better if we could include C-reactive protein [19,20], Vitamin D [21] and homocysteine level [22], which are considered CAD risk, directly or indirectly. Though not very evident, it is also important to explore whether genetic predisposition have any contribution to CAD [23,24].…”

Dietary antioxidants remodel DNA methylation patterns in chronic disease

“…The pattern of DNA methylation, established through dynamic DNA methylation and DNA demethylation, changes over the course of development and aberrant DNA methylation patterns have been linked to numerous human diseases, including chronic diseases (Barajas‐Olmos et al, ; Fernandez‐Sanles, Sayols‐Baixeras, Subirana, Degano, & Elosua, ; Lashley et al, ; Vucic et al, ).…”

“…Increasing evidence has revealed that DNA methylation has distinct roles in controlling gene expression of key players in atherosclerotic vascular tissues and consequently in CVD (Fernandez‐Sanles et al, ). The CpG island in the promoter region of oestrogen receptor α ( ERα ), a gene that protects against atherosclerosis through governing smooth muscle cell (SMC) proliferation, has consistently been found to be differentially methylated in atherosclerosis patients as compared to healthy controls (Huang, Zhi, & Wang, ).…”

“…In healthy tissue, ERα increases the expression of NOS, resulting in reduced SMC proliferation and platelet formation (Fernandez‐Sanles et al, ). During early atherogenesis, DNA hypermethylation of the ERα gene promoter contributes to gene silencing and as a consequence to the abnormally high proliferation of SMCs within atherosclerotic lesions (Fernandez‐Sanles et al, ). On the other hand, reduced DNA methylation in the promoter region of IL6 , a major player in the inflammation cascade, has been associated with greater production of cytokines from macrophages during atherogenesis (Yang, Zhao, Zhang, & Chen, ).…”

“…Unmethylated CpG sites within these regulatory regions enable binding of the transcriptional machinery, and gene is actively transcribed. On the other hand, methylation of the CpG sites in promoter or enhancer regions leads to recruitment of repressor complexes that prevent binding of the elements of the transcriptional machinery which results in gene silencing atherosclerotic vascular tissues and consequently in CVD (Fernandez-Sanles et al, 2017). The CpG island in the promoter region of oestrogen receptor α (ERα), a gene that protects against atherosclerosis through governing smooth muscle cell (SMC) proliferation, has consistently been found to be differentially methylated in atherosclerosis patients as compared to healthy controls (Huang, Zhi, & Wang, 2009).…”