DNA Methylation Aberrant in Atherosclerosis

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.

Automated summary

Atherosclerosis is a pathological process involving lipid oxidation, immune system activation, and endothelial dysfunction. DNA methylation, as one of the most important epigenetic mechanisms, plays a key role in the pathogenesis of atherosclerosis. This review discusses the abnormal changes of DNA methylation in atherosclerosis, including genome-wide hypermethylation with aging, hypermethylation linked to methyl supply and hyperhomocysteinemia, and the influence of oxidative stress on demethylation processes. The review also summarizes the current status of epigenetic treatment for atherosclerosis, providing new directions and potential therapeutic targets.