Abstract
Atherosclerosis (AS) is a pathological process involving lipid oxidation, immune system activation, and endothelial dysfunction. The activated immune system could lead to inflammation and oxidative stress. Risk factors like aging and hyperhomocysteinemia also promote the progression of AS. Epigenetic modifications, including DNA methylation, histone modification, and non-coding RNA, are involved in the modulation of genes between the environment and AS formation. DNA methylation is one of the most important epigenetic mechanisms in the pathogenesis of AS. However, the relationship between the progression of AS and DNA methylation is not completely understood. This review will discuss the abnormal changes of DNA methylation in AS, including genome-wide hypermethylation dominating in AS with an increase of age, hypermethylation links with methyl supply and generating hyperhomocysteinemia, and the influence of oxidative stress with the demethylation process by interfering with the hydroxyl-methylation of TET proteins. The review will also summarize the current status of epigenetic treatment, which may provide new direction and potential therapeutic targets for AS.
Highlights
Atherosclerosis (AS) is the pathological basis in heavy cardiovascular diseases like unstable angina pectoris, acute myocardial infarction, and abdominal aortic aneurysm (Tabas et al, 2015)
Wang et al (2018) collected various tissues from six patients who underwent coronary artery bypass surgery, including atherosclerotic plaques, great saphenous vein, and internal mammary artery. They have found that the genes which participated in immune response-associated pathways in AS were enriched by the hypomethylated genes
Epigenetic regulation has been observed in low-density lipoprotein oxidation—for example, the upregulated expression of DNMT1 causes methylation of the promoter region of Kruppel-like factor 2 (KLF2) in human umbilical vein endothelial cells (HUVECs) treated with oxidized low-density lipoprotein (Yan et al, 2017)
Summary
Atherosclerosis (AS) is a pathological process involving lipid oxidation, immune system activation, and endothelial dysfunction. The activated immune system could lead to inflammation and oxidative stress. Epigenetic modifications, including DNA methylation, histone modification, and non-coding RNA, are involved in the modulation of genes between the environment and AS formation. DNA methylation is one of the most important epigenetic mechanisms in the pathogenesis of AS. The relationship between the progression of AS and DNA methylation is not completely understood. This review will discuss the abnormal changes of DNA methylation in AS, including genomewide hypermethylation dominating in AS with an increase of age, hypermethylation links with methyl supply and generating hyperhomocysteinemia, and the influence of oxidative stress with the demethylation process by interfering with the hydroxyl-methylation of TET proteins.
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