METTL1 and cardiac hypertrophy: Loss of METTL1 and m7G modifications during senescence triggers rapid tRNA degradation, disrupts translation of key pathways, and activates stress responses that drive senescence phenotypes.[43] METTL1, upregulated in failing human and hypertrophic murine hearts, modulates cardiac hypertrophy via m7G modification of SRSF9 mRNA, enhancing SRSF9 expression and NFATc4 splicing.