胆汁酸与肠道菌群在原发性胆汁性胆管炎发生发展中的作用及机制
DOI: 10.12449/JCH260427
利益冲突声明:本文不存在任何利益冲突。
作者贡献声明:吴梦瑶负责文章的构思和论文撰写;潘佳茵、丁瑢负责论文框架的构建;李劲榆负责指导撰写文章;邰文琳负责最终版本修订,对论文整体负责。
Roles and mechanism of bile acids and gut microbiota in primary biliary cholangitis
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摘要: 原发性胆汁性胆管炎(PBC)是一种以肝内小胆管损伤为特征的胆汁淤积性自身免疫性肝病,其确切发病机制尚未完全阐明。近年来研究表明,胆汁酸代谢紊乱与肠道菌群失衡在PBC的发生与进展中扮演关键角色,二者通过“肠-肝轴”形成复杂的动态互作网络,协同调控免疫应答、代谢稳态以及炎症反应等核心生理病理过程。本文系统阐述了PBC中胆汁酸代谢与肠道菌群的异常特征,深入探讨其在PBC中的协同作用机制,并在此基础上提出联合靶向胆汁酸受体与调节肠道菌群的策略,有望突破现有治疗手段的局限,为PBC的临床干预提供新的思路与方向。Abstract: Primary biliary cholangitis (PBC) is a cholestatic autoimmune liver disease characterized by the injury of small intrahepatic bile ducts, and at present, the pathogenesis of PBC remains unclear. Recent studies have shown that bile acid metabolism disorder and gut microbiota imbalance play a key role in the development and progression of PBC, and they form a complex and dynamic interaction network via the “gut-liver axis” and regulate core physiopathological processes such as immune response, metabolic homeostasis, and inflammatory response in a synergistic manner. This article systematically elaborates on the abnormal features of bile acid metabolism and gut microbiota in PBC, discusses their synergistic mechanisms in PBC, and then proposes a combined strategy of targeting bile acid receptors and modulating gut microbiota, in order to overcome the limitations of current treatment modalities and provide new insights and directions for the clinical management of PBC.
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