METTL3-mediated mA 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. N-methyladenosine (mA) is one of the most prevalent RNA modifications, and methyltransferase-like 3 (METTL3), the core component of the mA 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 mA 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 mA-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.