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.心肌纤维化在心血管疾病中十分常见。N6-甲基腺嘌呤（N6-methyladenosine，m6A）是真核信使RNA（messenger RNA，mRNA）中最常见的修饰形式之一。既往研究表明，m6A修饰在心血管疾病中发挥关键调控作用。本研究通过转录组测序（RNA-seq）联合甲基化RNA免疫沉淀测序（MeRIP-seq）筛选得到FTO的潜在靶标。基于MeRIP-seq与RNA-seq的分析结果，FTO可抑制心脏成纤维细胞（CFs）中的胶原合成。