Abstract:Vascular remodeling refers to a series of structural and functional abnormalities in the vascular wall, which is characterized by stenosis of the lumen, thickening of the vascular wall, reduction of vascular elasticity and compliance caused by changes in the microenvironment inside and outside the blood vessel, and ultimately the occurrence of cardiovascular events. Although the prevention, diagnosis and intervention of clinical cardiovascular diseases have improved, vascular dysfunction caused by vascular remodeling is still a huge problem and challenge that plagues clinical efficacy. N6-methyladenosine (m6A) modification is the most common and abundant post-transcriptional modification type in eukaryotic RNA. m6A methyltransferase, m6A demethylase and m6A reading protein are responsible for the occurrence, deletion and recognition of m6A modification, respectively. The m6A modification regulates the fate of important transcripts by participating in the splicing, degradation, translation, and subcellular translocation of RNA target molecules, thereby playing a regulatory role in the maintenance of vascular physiological homeostasis and pathological remodeling. Studies have confirmed that m6A modification-mediated vascular endothelial cell (EC) dysfunction, phenotypic transformation,abnormal proliferation, migration of medial vascular smooth muscle cell (VSMC), and aggregation and activation of monocytes/macrophages are involved in the occurrence and development of vascular remodeling diseases such as atherosclerosis and aneurysms. This article reviews the recent literatures on m6A modification in vascular remodeling, and discusses the effect of m6A methylation modification of important target molecules related to vascular remodeling on vascular cells function. Based on these, the intervention of m6A methylation may be a new target for clinical treatment and diagnosis in the future.
