N6-methyladenosine (m6A) RNA methylation is an emerging area of epigenetics, which is a reversible and dynamic modification mediating by ‘writers’ (methylase, adding methyl groups, METTL3, METTL14, and WTAP), ‘erasers’ (demethylase, deleting methyl groups, FTO and ALKBH5), and ‘readers’ (YTHDF1-3, YTHDC1 and YTHDC2). Recent studies in human, animal models and cell levels have disclosed a critical role of m6A modification in regulating the homeostasis of metabolic processes and cardiovascular function. Evidence from these studies identify m6A as a candidate of biomarker and therapeutic target for metabolic abnormality and cardiovascular diseases (CVD). Comprehensive understanding of the complexity of m6A regulation in metabolic diseases and CVD will be helpful for us to understand the pathogenesis of CVD. In this review, we discuss the regulatory role of m6A in metabolic abnormality and CVD. We will emphasize the clinical relevance of m6A dysregulation in CVD.

N6-甲基腺苷 (m6A) RNA 甲基化是表观遗传学的一个新兴领域，它是由“作家”（甲基化酶，添加甲基、METTL3、METTL14 和 WTAP）、“橡皮擦”（去甲基化酶，删除甲基）介导的可逆和动态修饰。组、FTO 和 ALKBH5）和“读者”（YTHDF1-3、YTHDC1 和 YTHDC2）。最近在人类、动物模型和细胞水平上的研究揭示了 m6A 修饰在调节代谢过程和心血管功能的稳态方面的关键作用。这些研究的证据表明 m6A 是代谢异常和心血管疾病 (CVD) 的候选生物标志物和治疗靶点。全面了解 m6A 调控在代谢性疾病和 CVD 中的复杂性，将有助于我们了解 CVD 的发病机制。在这次审查中，我们讨论了 m6A 在代谢异常和 CVD 中的调节作用。我们将强调 m6A 失调在 CVD 中的临床相关性。