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Cigarette smoking remains a worldwide health epidemic. In the United States, despite the well-established risks, cigarette smoking remains the leading cause of preventable disease and death accounting for >480 000 deaths annually, with 1 in every 3 of such deaths related to cardiovascular diseases (CVD).1 For every patient who dies because of smoking, at least 30 people live with a serious smoking-related illness,1 including ischemic heart disease, stroke, and peripheral vascular disease, etc. Although cigarette smoking has declined during the past decade among US adults from 20.9% in 2005 to 17.8% in 2013, an estimated 42.1 million adults in the US remain current smokers.2 In lieu of these sobering statistics, it remains imperative to better understand the molecular mechanisms by which smoking drives the development of CVD. Such insights, particularly when considering smoking as a mediator of accelerated atherosclerosis, may provide both preclinical diagnostic biomarkers and drug targets for therapeutics of CVD among smokers and nonsmokers alike.Article see p 707 Recent studies have shown that smoking is highly associated with both genome-wide epigenetic cytosine-(phosphate)-guanine (CpG) DNA methylation alterations and downstream transcriptome changes.3–6 Among such effects, coordinated DNA methylation and gene expression alteration of the Aryl Hydrocarbon Receptor Repressor ( AHRR ) in various cell types is the most significant and robust change associated with smoking.6–8 Maternal smoking has been consistently shown to be associated with DNA methylation change of AHRR in …

Aryl Hydrocarbon Receptor Repressor Methylation