Inflammatory bowel disease (IBD) including Crohn’s disease (CD) and ulcerative colitis (UC) seriously affects the quality of life for patients. The pathogenesis of IBD contains the environmental, host genetic and epigenetic factors. In recent years, the studies of protein ubiquitination, an important protein post-translational modification as an epigenetic factor, have emerged in the pathogenesis and development of IBD. In the past few years, accumulative evidence illustrated that six E3 ubiquitin ligases, namely, ring finger protein (RNF) 183, RNF 20, A20, Pellino 3, TRIM62 and Itch, exhibited clear mechanisms in the development of IBD. They regulate the intestinal inflammation by facilitating the ubiquitination of targeted proteins which participate in different inflammatory signaling pathways. Besides, it was reported that some deubiquitinating enzymes such as Cylindromatosis and USP7 were involved in the development of IBD, but the molecular mechanism was still unclear. This review summarized the role and regulatory mechanism of protein ubiquitination in the pathogenesis and development of IBD, providing insights to develop a new therapeutic strategy in IBD treatments.

包括克罗恩病 (CD) 和溃疡性结肠炎 (UC) 在内的炎症性肠病 (IBD) 严重影响患者的生活质量。IBD的发病机制包括环境因素、宿主遗传因素和表观遗传因素。近年来，蛋白质泛素化作为一种​​重要的蛋白质翻译后修饰作为表观遗传因子，在IBD的发病和发展中出现。近年来，越来越多的证据表明，6种E3泛素连接酶，即环指蛋白（RNF）183、RNF 20、A20、Pellino 3、TRIM62和Itch，在IBD的发生发展中表现出明确的机制。它们通过促进参与不同炎症信号通路的靶蛋白的泛素化来调节肠道炎症。除了，据报道，一些去泛素化酶如圆柱瘤病和USP7参与了IBD的发展，但分子机制尚不清楚。该综述总结了蛋白质泛素化在 IBD 发病机制和发展中的作用和调控机制，为开发 IBD 治疗的新治疗策略提供了见解。