N6-Adenosine Methylation (m6A) RNA Modification: an Emerging Role in Cardiovascular Diseases

N6-methyladenosine (m(6)A) is the most abundant and prevalent epigenetic modification of mRNA in mammals. This dynamic modification is regulated by m(6)A methyltransferases and demethylases, which control the fate of target mRNAs through influencing splicing, translation and decay. Recent studies suggest that m(6)A modification plays an important role in the progress of cardiac remodeling and cardiomyocyte contractile function. However, the exact roles of m(6)A in cardiovascular diseases (CVDs) have not been fully explained. In this review, we summarize the current roles of the m(6)A methylation in the progress of CVDs, such as cardiac remodeling, heart failure, atherosclerosis (AS), and congenital heart disease. Furthermore, we seek to explore the potential risk mechanisms of m(6)A in CVDs, including obesity, inflammation, adipogenesis, insulin resistance (IR), hypertension, and type 2 diabetes mellitus (T2DM), which may provide novel therapeutic targets for the treatment of CVDs.

Automated summary

N6-methyladenosine (m(6)A) is the most abundant and prevalent epigenetic modification of mRNA in mammals, regulating the fate of target mRNAs by influencing splicing, translation, and decay. Its important role in cardiovascular diseases, such as cardiac remodeling, heart failure, atherosclerosis, and congenital heart disease, has been highlighted in recent studies, although the exact mechanisms are not fully elucidated.