Abstract
N(6)-methyladenosine (m(6)A) modification is a newly discovered regulatory mechanism in eukaryotes. As one of the most common epigenetic mechanisms, m(6)A's role in the development of atherosclerosis (AS) and atherosclerotic diseases (AD) has also received increasing attention. Herein, we elucidate the effect of m(6)A on major risk factors for AS, including lipid metabolism disorders, hypertension, and hyperglycemia. We also describe how m(6)A methylation contributes to endothelial cell injury, macrophage response, inflammation, and smooth muscle cell response in AS and AD. Subsequently, we illustrate the m(6)A-mediated aberrant biological role in the pathogenesis of AS and AD, and analyze the levels of m(6)A methylation in peripheral blood or local tissues of AS and AD, which helps to further discuss the diagnostic and therapeutic potential of m(6)A regulation for AS and AD. In summary, studies on m(6)A methylation provide new insights into the pathophysiologic mechanisms of AS and AD, and m(6)A methylation could be a novel diagnostic biomarker and therapeutic target for AS and AD.