Key role of m6A methylation in sarcopenia

• METTL3-mediated m6A methylation is crucial for maintaining the differentiation potential of myogenic cells. • The METTL3/14-m6A-YTHDF1/2 axis regulates satellite cells, promoting myoblast proliferation and myogenic differentiation. • Elevating m6A methylation levels can alleviate the atrophic phenotype of denervated skeletal muscle. • The precise regulatory targets and synergistic mechanisms of m6A reader proteins in sarcopenia remain unclear, and clinical validation is lacking.