Regulation of m6A methylation in the immune microenvironment in the development of diabetes mellitus

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Diabetes mellitus is a widespread metabolic disorder characterized by chronic hyperglycemia, driven primarily by insulin resistance and β-cell dysfunction. N6-methyladenosine (m6A), the most prevalent internal RNA modification in eukaryotes, has emerged as a critical regulator in diabetes pathogenesis. This review outlines how m6A methylation, mediated by writers (METTL3, METTL14), erasers (FTO, ALKBH5), and readers (YTHDFs, IGF2BPs), influences key diabetic processes including β-cell function, lipid metabolism, and insulin resistance. A key focus is on the role of m6A in modulating the immune microenvironment, such as by regulating macrophage polarization and T-cell activity, which contributes to inflammation and disease progression in both type 1 and type 2 diabetes. Furthermore, m6A dysregulation is implicated in multiple diabetic complications. Therapeutic agents, including existing drugs, natural extracts, and specific m6A inhibitors, can modulate m6A levels, highlighting its potential as a therapeutic target. This review synthesizes the evidence linking m6A to diabetes, with an emphasis on immunoregulation, and suggests that targeting m6A pathways offers promise for future treatments.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

Browse all related research

Filter the research library by this study's title keywords, author, or publication year.