Mettl3-Mediated m⁶A Modification of Fgf16 Restricts Cardiomyocyte Proliferation during Heart Regeneration

To study m6A function in heart regeneration, investigators modulated Mettl3 expression in vitro and in vivo. Knockdown of Mettl3 significantly increased the proliferation of cardiomyocytes and accelerated heart regeneration following heart injury in neonatal and adult mice.