METTL3-mediated m⁶A methylation: implications for diabetes pathogenesis and therapeutic potential

Diabetes mellitus is a complex, chronic metabolic disease with a multifactorial pathogenesis involving genetic predisposition and environmental factors. Recently, epigenetics, particularly RNA methylation modifications, have gained increasing attention. N⁶-methyladenosine (m⁶A) is one of the most prevalent RNA modifications, and methyltransferase-like 3 (METTL3), the core component of the m⁶A methyltransferase complex, plays a pivotal role in regulating key physiological and pathological processes, including islet β-cell function, insulin regulation, and glucose metabolism. This article reviews the mechanisms by which METTL3 and m⁶A modifications contribute to the development of diabetes and its complications. Preclinical studies suggest METTL3 a promising target, but future research should focus on identifying safe, effective regulatory strategies for its clinical application. Overall, METTL3 and its m⁶A-mediated modifications present promising novel therapeutic targets for the prevention and treatment of diabetes mellitus, providing novel theoretical insights and strategies for managing the disease and its complications.