Schematic representation of the proposed effect of hyperhomocysteinemia on DNA methylation and atherosclerosis. SAH indicates S-adenosyl-homocysteine; DNMT, DNA methyltransferase. Hcy may induce the accumulation of SAH, a potent inhibitor of cellular methylation, as well as subsequent cellular hypomethylation, including DNA hypomethylation. Hcy-induced DNA demethylation is mediated by DNMT1 inactivation, which leads to demethylation of the cyclin A promoter CDE, and also leads to cyclin A promoter remodeling. Cyclin A chromatin remodeling may facilitate the function of CDE suppressor and result in cyclin A suppression. The activity of the suppressor element is increased due to DNA hypomethylation, which promotes chromatin remodeling and the access of suppressors to the chromatin, leading to transcriptional inhibition.

Schematic representation of the proposed effect of hyperhomocysteinemia on DNA methylation and atherosclerosis. SAH indicates S-adenosyl-homocysteine; DNMT, DNA methyltransferase. Hcy may induce the accumulation of SAH, a potent inhibitor of cellular methylation, as well as subsequent cellular hypomethylation, including DNA hypomethylation. Hcy-induced DNA demethylation is mediated by DNMT1 inactivation, which leads to demethylation of the cyclin A promoter CDE, and also leads to cyclin A promoter remodeling. Cyclin A chromatin remodeling may facilitate the function of CDE suppressor and result in cyclin A suppression. The activity of the suppressor element is increased due to DNA hypomethylation, which promotes chromatin remodeling and the access of suppressors to the chromatin, leading to transcriptional inhibition.

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