FTO suppresses cardiac fibrosis after myocardial infarction via m6A-mediated epigenetic modification

Cardiac fibrosis is common in cardiovascular diseases. N6-methyladenosine (m6A) is one of the most common modifications in eukaryotic mRNAs. Previous research has suggested that m6A modification is vital in cardiovascular diseases. The underlying targets of FTO were selected through transcriptome sequencing (RNA-seq) combined with methylated RNA immunoprecipitation sequencing (MeRIP-seq). According to MeRIP-seq and RNA-seq, FTO inhibited collagen synthesis in CFs. Overall design: Neonatal rat cardiac fibroblasts (NRCFs) were collected from healthy Sprague-Dawley rats within 3 days post-birth. NRCFs were transfected with the plasmid of FTO and Vector and performed comparative gene expression profiling between FTO and Vector groups.