Abstract
Cardiovascular disease is currently the leading cause of death worldwide, and its underlying regulatory mechanisms remain largely unknown. N(6)-Methyladenosine (m(6)A) RNA methylation is an epigenetic modification involved in the splicing, nuclear export, translational regulation, and degradation of RNA. After the initial identification of m(6)A RNA methylation in 1974, the rise of next-generation sequencing technology to detect m(6)A throughout the transcriptome led to its renewed recognition in 2012. Since that time, m(6)A methylation has been extensively studied, and its functions, mechanisms, and effectors (e.g., METTL3, FTO, METTL14, WTAP, ALKBH5, and YTHDFs) in various diseases, including cardiovascular diseases, have rapidly been investigated. In this review, we first examine and summarize the molecular and cellular functions of m(6)A methylation and its readers, writers, and erasers in the cardiovascular system. Finally, we discuss future directions for m(6)A methylation research and the potential for therapeutic targeting of m(6)A modification in cardiovascular disease.