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

Abstract

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 (m6A) is the most abundant modification in eukaryotic RNA molecules and plays a critical role in regulating RNA metabolism. Dysregulation of m6A modification has been linked to a variety of diseases. Interestingly, aberrant expression of m6A-associated factors is observed in AD. The m6A methylation can promote or inhibit the development of AD by modulating cell death, oxidative stress, macrophage polarization and VSMC phenotype switching, depending on m6A-modified transcripts, readers and downstream pathways. In addition, m6A exerts a significant effect on the major risk factors for AD, including hypertension, atherosclerosis, obesity and aortic aneurysm. Thus, modulating m6A 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 m6A modification and its regulators. Subsequently, we summarize the recent research progress on the role of m6A in AD and related-risk factors, with an emphasis on its diagnostic value and therapeutic potential.

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