The potential roles of RNA N6-methyladenosine in atherosclerosis.

Abstract

Atherosclerosis, characterized by endothelial injury, multicellular involvement, chronic inflammation, and lipid deposition, can lead to acute cardiovascular events. N6-methyladenosine (m6A) is the most abundant, prevalent RNA modification in mammalian cells. m6A, a reversible modification, can be catalyzed by m6A methyltransferase complexes (writers), reverted by demethylases (erasers), and recognized by m6A-binding proteins (readers). Emerging evidence suggests that m6A modification plays a significant role in regulating many biological and cellular processes in atherosclerosis. In this review, we highlight the biological function of m6A modification and give a brief perspective on its future applications in atherosclerosis. This is a narrative review. The literature search strategy for indexed Scopus articles was performed randomly using PubMed and MEDLINE as the primary sources. No specific term was used. As the mechanism of the relationship between inflammatory response and atherosclerosis, m6A has become a new focus in the study of clinical treatment strategies for atherosclerosis. METTL14-dependent m6A modification may be a target for atherosclerosis therapy. A variety of m6A regulatory factors promote the progression of atherosclerosis by regulating polarization and inflammation of macrophages. WTAP and METTL14 can affect the phenotypic modulation of VSMCs through m6A modification. The existence of m6A in cardiovascular transcripts is necessary to maintain cardiac function, and the level of m6A modification is increased in a variety of atherosclerotic vascular cells, indicating that m6A modification is involved in the pathophysiological process of atherosclerosis. m6A modification plays an important character in atherosclerosis.