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Abstract: The onset of inflammatory bowel disease (IBD) involves many factors, including environmental parameters, microorganisms, and the immune system. Although research on IBD continues to expand, the specific pathogenesis mechanism is still unclear. protein modification refers to chemical modification after protein biosynthesis, also known as post-translational modification (PTM), which causes changes in the properties and functions of proteins. Since proteins can be modified in different ways, such as acetylation, methylation, and phosphorylation, the functions of proteins in different modified states will also be different. Transitions between different states of protein or changes in modification sites can regulate protein properties and functions. Such modifications like neddylation, sumoylation, glycosylation, and acetylation can activate or inhibit various signaling pathways (e.g., nuclear factor-‍κB (NF-‍κB), extracellular signal-regulated kinase (ERK), and protein kinase B (AKT)) by changing the intestinal flora, regulating immune cells, modulating the release of cytokines such as interleukin-1β (IL-‍‍1β), tumor necrosis factor-α(TNF‍-‍α), and interferon-‍γ(IFN-‍γ), and ultimately leading to the maintenance of the stability of the intestinal epithelial barrier. In this review, we focus on the current understanding of PTM and describe its regulatory role in the pathogenesis of IBD.

蛋白质修饰在炎症性肠病中作用研究进展

摘要：炎症性肠病（inflammatory bowel disease，IBD）的发病涉及许多因素，包括环境、微生物和免疫系统的改变。尽管对IBD的研究不断深入，但具体的发病机制尚不清楚。蛋白质修饰是指蛋白质生物合成后的化学修饰，也称为翻译后修饰（post-translational modification，PTM），使蛋白质的性质和功能发生变化。由于蛋白质可以通过乙酰化、甲基化和磷酸化等不同方式进行修饰，因此不同修饰状态的蛋白质的功能也会有所不同。蛋白质不同状态之间的转换或修饰位点的变化可以调节蛋白质的特性和功能，如NEDD8蛋白修饰、SUMO化修饰、糖基化和乙酰化等修饰可以通过改变肠道菌群、调节免疫细胞、调节细胞因子（如IL-1β、TNF-α、IFN-γ），最终维持肠上皮屏障的稳定性。在这篇综述中，我们关注当前对PTM的理解，并描述其在IBD发病机制中的调节作用。

关键词：炎症性肠病（IBD）；蛋白质修饰；NEDD8蛋白修饰；SUMO化修饰；糖基化；乙酰化

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