Although the exact cause of inflammatory bowel disease (IBD) is still unknown, there is a lot of evidence to support the notion that it results from a combination of environmental factors, immune system issues, gut microbial changes, and genetic susceptibility. In recent years, the role of epigenetics in the pathogenesis of IBD has drawn increasing attention. The regulation of IBD-related immunity, the preservation of the intestinal epithelial barrier, and autophagy are all significantly influenced by epigenetic factors. The most extensive epigenetic methylation modification of mammalian mRNA among them is N6-methyladenosine (m⁶A). It summarizes the general structure and function of the m⁶A regulating factors, as well as their complex effects on IBD by regulating the intestinal mucous barrier, intestine mucosal immunity, epidermal cell death, and intestinal microorganisms.This paper provides key insights for the future identification of potential new targets for the diagnosis and treatment of IBD.

尽管炎症性肠病 (IBD) 的确切病因尚不清楚，但有大量证据支持这一观点，即它是环境因素、免疫系统问题、肠道微生物变化和遗传易感性综合作用的结果。近年来，表观遗传学在IBD发病机制中的作用日益受到关注。IBD相关免疫的调节、肠上皮屏障的保存和自噬均受到表观遗传因素的显着影响。其中最广泛的哺乳动物mRNA表观遗传甲基化^{修饰是N6-甲基腺苷(m 6} A)。^{它总结了 m 6} A 调节因子的一般结构和功能，以及它们通过调节肠粘膜屏障、肠粘膜免疫、表皮细胞死亡和肠道微生物对 IBD 的复杂影响。本文为未来提供了重要见解确定诊断和治疗 IBD 的潜在新靶点。