Abstract
N(6)-methyladenosine (m(6)A) methylation is one of the most predominant internal RNA modifications in eukaryotes and has become a hot spot in the field of epigenetics in recent years. Cardiovascular diseases (CVDs) are a leading cause of death globally. Emerging evidence demonstrates that RNA modifications, such as the m(6)A modification, are associated with the development and progression of many diseases, including CVDs. An increasing body of studies has indicated that programmed cell death (PCD) plays a vital role in CVDs. However, the molecular mechanisms underlying m(6)A modification and PCD in CVDs remain poorly understood. Herein, elaborating on the highly complex connections between the m(6)A mechanisms and different PCD signaling pathways and clarifying the exact molecular mechanism of m(6)A modification mediating PCD have significant meaning in developing new strategies for the prevention and therapy of CVDs. There is great potential for clinical application.