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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

吴梦瑶 潘佳茵 丁瑢 李劲榆 邰文琳

引用本文:
Citation:

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
基金项目: 

国家自然科学基金 (82060385);

国家自然科学基金 (82560413);

云南省基础研究计划昆医联合专项面上项目 (202201AY070001-099)

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。
详细信息
    通信作者:

    邰文琳, taiwenlin@kmmu.edu.cn (ORCID: 0000-0002-8278-929X)

Roles and mechanism of bile acids and gut microbiota in primary biliary cholangitis

Research funding: 

National Natural Science Foundation of China (82060385);

National Natural Science Foundation of China (82560413);

General Project of the Joint Special Program between Kunming Medical University and Yunnan Provincial Basic Research Plan (202201AY070001-099)

More Information
  • 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。

     

  • 注: MDSC,髓源性抑制细胞;CX3CL1,趋化因子CX3C配体1;REG3γ,再生胰岛衍生蛋白3γ;PDC-E2,线粒体丙酮酸脱氢酶复合体E2亚单位。

    图  1  “肠-肝轴”在PBC发生发展中的作用机制

    Figure  1.  Mechanism of the gut-liver axis in the development of PBC

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  • 收稿日期:  2025-06-21
  • 录用日期:  2025-10-27
  • 出版日期:  2026-04-25
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