Cardiovascular Mettl3 Deficiency Causes Congenital Cardiac Defects and Postnatal Lethality in Mice.

ABSTRACT: N⁶-methyladenosine (m⁶A) is the most common epigenetic modification of RNA, but whether m⁶A RNA methylation modulates cardiovascular development or congenital heart diseases (CHDs) has not been determined. The published high-throughput sequencing data suggested that transcripts of genes related to CHDs were prone to m⁶A modification, while the expression of methyltransferase-like 3 (METTL3)-involved methyltransferase complex was downregulated in mouse embryonic hearts following prenatal alcohol exposure as a critical CHD risk factor, indicating the association of insufficient m⁶A RNA methylation with CHDs. Using cardiovascular-specific Mettl3 knockout mice (Tagln-Cre; Mettl3^flox/flox ), we observed that

SUBMITTER: Feng Q 

PROVIDER: S-EPMC12035893 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature