作者: John W. Cole , Huichun Xu
DOI: 10.1161/CIRCGENETICS.115.001243
关键词: Stroke 、 Disease 、 Vascular disease 、 Genetics 、 CpG site 、 Biology 、 Methylation 、 Bioinformatics 、 Aryl hydrocarbon receptor repressor 、 DNA methylation 、 Epigenetics
摘要: Cigarette smoking remains a worldwide health epidemic. In the United States, despite well-established risks, cigarette leading cause of preventable disease and death accounting for >480 000 deaths annually, with 1 in every 3 such related to cardiovascular diseases (CVD).1 For patient who dies because smoking, at least 30 people live serious smoking-related illness,1 including ischemic heart disease, stroke, peripheral vascular etc. Although has declined during past decade among US adults from 20.9% 2005 17.8% 2013, an estimated 42.1 million remain current smokers.2 lieu these sobering statistics, it imperative better understand molecular mechanisms by which drives development CVD. Such insights, particularly when considering as mediator accelerated atherosclerosis, may provide both preclinical diagnostic biomarkers drug targets therapeutics CVD smokers nonsmokers alike. Article see p 707 Recent studies have shown that is highly associated genome-wide epigenetic cytosine-(phosphate)-guanine (CpG) DNA methylation alterations downstream transcriptome changes.3–6 Among effects, coordinated gene expression alteration Aryl Hydrocarbon Receptor Repressor ( AHRR ) various cell types most significant robust change smoking.6–8 Maternal been consistently be …