Endothelial cells undergo gene expression changes when exposed to disturbed blood flow. The dysfunctional endothelial cells perpetuate plaque development. DNA methylation has been implicated as a risk factor in atherosclerosis in smooth muscle cells.
Hypermethylation of the estrogen receptor, a promoter, and high homocysteine levels, a source of the methyl group used for DNA methylation were found in atherosclerosis patients. Regulation of the gene’s cAMP response, the master switch, can be reset so the gene can be returned to normal.