细胞焦亡: 连接肠道菌群与肝脏疾病的新桥梁
DOI: 10.12449/JCH240930
利益冲突声明:本文不存在任何利益冲突。
作者贡献声明:赵奕杰负责拟定写作思路,撰写文章;谢露负责调整文章架构和修改;张亚亭负责文献收集整理;刘光伟指导文章撰写和修改。
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摘要: 自肠-肝轴的概念被提出以来,已有大量研究着眼于探索肠道菌群和肝病之间的联系,但以细胞焦亡为枢纽,探究肠-肝串扰的内在机制的观点仍处于萌芽阶段。本文主要通过叙述了肠道菌群失调通过影响黏膜屏障的完整性和胆汁酸的代谢,诱导细胞焦亡,进而影响肝脏相关疾病的发生和进展的过程,并总结出肠道菌群失调通过诱导NLRP3/AIM2/Caspase-1依赖型、Caspase-4/11/GSDMD依赖型和Caspase-3/GSDME依赖型细胞焦亡以影响肝脏相关疾病的观点。希望通过建立细胞焦亡与肠-肝免疫串扰之间的联系,为未来肝病的诊治提供新的思路和靶点。Abstract: Since the proposal of the concept of the gut-liver axis, a large number of studies have focused on exploring the connection between gut microbiota and liver disease; however, the idea of using pyroptosis as a hub to explore the intrinsic mechanism of gut-liver crosstalk is still in its infancy. This article mainly describes the process by which gut microbiota dysbiosis affects the integrity of mucosal barrier and bile acid metabolism, induces pyroptosis, and thereby affects the development and progression of liver diseases, and it also concludes that gut microbiota dysbiosis affects liver diseases by inducing NLRP3/AIM2/Caspase-1-dependent, Caspase-4/11/GSDMD-dependent, and Caspase-3/GSDME-dependent pyroptosis. In summary, this study aims to provide new ideas and targets for the future diagnosis and treatment of liver diseases by establishing the connection between pyroptosis and intestinal-liver immune crosstalk.
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Key words:
- Liver Diseases /
- Gastrointestinal Microbiome /
- Pyroptosis /
- Bile Acids and Salts
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