间充质干细胞通过泛素化减轻炎症性肠病的作用

Hong Xi Liao, Xiaojun Mao, Lan Wang, Naijian Wang, D. K. W. Ocansey, Bo Wang, Fei Mao
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引用次数: 0

摘要

炎症性肠病(IBD)是一种消化道疾病,也是自身免疫性疾病的一种,正在成为全球公共卫生关注的重大疾病和沉重的临床负担。有文献记载,多种信号通路可调节 IBD,但确切的激活和调控机制尚未完全阐明;因此,需要不断探索在 IBD 发展过程中发挥关键作用的分子和通路。近年来,一些蛋白质翻译后修饰途径,如泛素化、磷酸化、甲基化、乙酰化和糖酵解,都与 IBD 有关。IBD中泛素化异常通常与免疫反应失调和炎症有关。间充质干细胞(MSCs)在通过泛素-蛋白酶体系统(一种负责蛋白质降解的细胞机制)调节泛素化修饰方面发挥着至关重要的作用。具体而言,研究表明间充质干细胞可影响参与炎症通路的关键信号分子的泛素化。本文回顾了间充质干细胞调控泛素化在 IBD 中的最新研究进展,强调了间充质干细胞在治疗 IBD 中的治疗潜力,并为开发有针对性的干预措施以调节免疫系统和缓解炎症状况提供了一条前景广阔的途径。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The role of mesenchymal stem cells in attenuating inflammatory bowel disease through ubiquitination
Inflammatory bowel disease (IBD), a condition of the digestive tract and one of the autoimmune diseases, is becoming a disease of significant global public health concern and substantial clinical burden. Various signaling pathways have been documented to modulate IBD, but the exact activation and regulatory mechanisms have not been fully clarified; thus, a need for constant exploration of the molecules and pathways that play key roles in the development of IBD. In recent years, several protein post-translational modification pathways, such as ubiquitination, phosphorylation, methylation, acetylation, and glycolysis, have been implicated in IBD. An aberrant ubiquitination in IBD is often associated with dysregulated immune responses and inflammation. Mesenchymal stem cells (MSCs) play a crucial role in regulating ubiquitination modifications through the ubiquitin-proteasome system, a cellular machinery responsible for protein degradation. Specifically, MSCs have been shown to influence the ubiquitination of key signaling molecules involved in inflammatory pathways. This paper reviews the recent research progress in MSC-regulated ubiquitination in IBD, highlighting their therapeutic potential in treating IBD and offering a promising avenue for developing targeted interventions to modulate the immune system and alleviate inflammatory conditions.
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