The emerging role of m6A in aortic dissection: from molecular mechanisms to therapeutic potential

Aortic dissection (AD) is an emergent medical condition with a hidden onset and sudden rupture, which usually results in a high mortality rate. N6-methyladenosine (m 6 A) is the most abundant modification in eukaryotic RNA molecules and plays a critical role in regulating RNA metabolism. Dysregulation of m 6 A modification has been linked to a variety of diseases. Interestingly, aberrant expression of m 6 A-associated factors is observed in AD. The m 6 A methylation can promote or inhibit the development of AD by modulating cell death, oxidative stress, macrophage polarization and VSMC phenotype switching, depending on m 6 A-modified transcripts, readers and downstream pathways. In addition, m 6 A exerts a significant effect on the major risk factors for AD, including hypertension, atherosclerosis, obesity and aortic aneurysm. Thus, modulating m 6 A modification by small-molecule inhibitors, natural products or miRNAs may represent a promising approach for developing new therapeutic interventions for AD. In this review, we first give a brief perspective on m 6 A modification and its regulators. Subsequently, we summarize the recent research progress on the role of m 6 A in AD and related-risk factors, with an emphasis on its diagnostic value and therapeutic potential.