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肠道菌群在慢加急性肝衰竭中的变化特征及致病机制

陈桂容 王明刚 林华明 严惠萍 王秀峰

引用本文:
Citation:

肠道菌群在慢加急性肝衰竭中的变化特征及致病机制

DOI: 10.3969/j.issn.1001-5256.2023.08.034
基金项目: 

广西自然科学基金 (2018GXNSFGA281002);

广西自然科学基金 (2018GXNSFBA281031);

广西研究生教育创新计划项目 (YCSY2022027)

利益冲突声明: 本文不存在任何利益冲突。
作者贡献声明: 陈桂容、王明刚、王秀峰对文章的思路及设计有关键贡献;陈桂容负责拟定写作框架并撰写文章;林华明、严惠萍均参与了文献检索及论文修订;王明刚、王秀峰负责指导修改并最终定稿。
详细信息
    通信作者:

    王秀峰,52912236@qq.com (ORCID: 0000-0003-0841-5908)

Changes and pathogenic mechanism of intestinal flora in acute-on-chronic liver failure

Research funding: 

Natural Science Foundation of Guangxi Zhuang Autonomous Region (2018GXNSFGA281002);

Natural Science Foundation of Guangxi Zhuang Autonomous Region (2018GXNSFBA281031);

Guangxi Postgraduate Education Innovation Program (YCSY2022027)

More Information
    Corresponding author: WANG Xiufeng, 52912236@qq.com (ORCID: 0000-0003-0841-5908)
  • 摘要: 慢加急性肝衰竭起病迅速而病死率高,预后差,且缺乏特异性药物治疗及手段。近年来,越来越多的证据表明肠道微生物群对维持人体微环境稳态的作用至关重要。利用宏基因组学全面测试肠道菌群特征可证明肠道菌群与慢性肝脏疾病发生发展方面存在交互关联。在慢加急性肝衰竭发病机制研究中,发现肠道微生物群在其致病过程中扮演重要角色。基于此,本文总结了慢加急性肝衰竭发生发展过程中肠道菌群的变化特征及其参与致病的机制途径,以期从肠道菌群调控新视角为慢加急性肝衰竭的临床治疗提供新靶点。

     

  • 图  1  肠道菌群激活LPS/TLR4信号通路在肝脏中的作用机制示意图

    Figure  1.  Schematic figure of the mechanism of intestinal flora activating LPS/TLR4 signaling pathway in the liver

    图  2  肠道菌群参与胆汁酸异常代谢机制示意图

    注:CHOL,胆固醇;CYP450/CYP7A1,细胞色素P450酶/胆固醇7α-羟化酶;BSEP,胆盐输出泵;CDCA/CA:鹅去氧胆酸/胆酸;7α-dehydroxylase,7α-脱羟基酶;LCA/DCA/UDCA,石胆酸/去氧胆酸/熊去氧胆酸。

    Figure  2.  Schematic figure of intestinal flora involved in abnormal bile acid metabolism

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  • 收稿日期:  2022-10-24
  • 录用日期:  2022-12-08
  • 出版日期:  2023-08-20
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