Mettl3-mediated m⁶A modification of Fgf16 restricts cardiomyocyte proliferation during heart regeneration.

ABSTRACT: Cardiovascular disease is the leading cause of death worldwide due to the inability of adult heart to regenerate after injury. N⁶-methyladenosine (m⁶A) methylation catalyzed by the enzyme methyltransferase-like 3 (Mettl3) plays an important role in various physiological and pathological bioprocesses. However, the role of m⁶A in heart regeneration remains largely unclear. To study m⁶A function in heart regeneration, we 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. However, Mettl3 overexpression decreased cardiomyocyte proliferation and suppressed heart regener

SUBMITTER: Jiang FQ 

PROVIDER: S-EPMC9674341 | biostudies-literature | 2022 Nov

REPOSITORIES: biostudies-literature