Atherosclerosis: an epigenetic balancing act that goes wrong

Increasing evidence points to dietary lipids and their derivates as dynamic modulators of pro- or anti-inflammatory gene expression pathways via their ability to interact with nuclear receptors that are central to the regulation of numerous biological functions, including lipid metabolism, inflammatory mediator production, and vascular homeostasis. The biological effects of these receptors are the result of a finely tuned equilibrium between gene activation and repression, resulting from their ability to switch between chromatin-remodelling co-repressor and co-activator partners. The aim of this review is to discuss the concept that selected dietary components induce an atherosclerotic cellular phenotype, at least in part, by imposing epigenetic marks that shift the physiologic program of differential gene activation and repression. Aberrant epigenetic marks are seeded in promoter sequences as well as in intragenic sequences where they might regulate transcript splicing.