m6A mRNA methylation: Biological features, mechanisms, and therapeutic potentials in type 2 diabetes mellitus

Summary As the most common internal post‐transcriptional RNA modification in eukaryotic cells, N6‐methyladenosine (m 6 A) performs a dynamic and reversible role in a variety of biological processes mediated by methyltransferases (writers), demethylases (erasers), and m 6 A binding proteins (readers). M 6 A methylation enables transcriptome conversion in different signals that regulate various physiological activities and organ development. Over the past few years, emerging studies have identified that mRNA m 6 A regulators defect in β‐cell leads to abnormal regulation of the target mRNAs, thereby resulting in β‐cell dysfunction and loss of β‐cell identity and mass, which are strongly associated with type 2 diabetes mellitus (T2DM) pathogenesis. Also, mRNA m 6 A modification has been implicated with insulin resistance in muscles, fat, and liver cells/tissues. In this review, we elaborate on the biological features of m 6 A methylation; provide a comprehensive overview of the underlying mechanisms that how it controls β‐cell function, identity, and mass as well as insulin resistance; highlight its connections to glucose metabolism and lipid metabolism linking to T2DM; and further discuss its role in diabetes complications and its therapeutic potentials for T2DM diagnosis and treatment.