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肝性脑病发病机制中的多器官交互作用

赵子昕 祝叶青 叶存心 宋卓芫 宋冬

引用本文:
Citation:

肝性脑病发病机制中的多器官交互作用

DOI: 10.12449/JCH260533
基金项目: 

2022年度江苏高校哲学社会科学研究一般项目 (2022SJYB1865);

南京医科大学2023年度教育研究课题一般项目 (2023ZC104);

南京医科大学康达学院第二期“科研人才培养计划” (KD2022KYRC012)

利益冲突声明:本文不存在任何利益冲突。
作者贡献声明:赵子昕负责拟定文章思路,并起草和修改文章的关键内容;祝叶青负责搜集参考文献;叶存心负责图片制作;宋卓芫负责文章格式修改与投稿;宋冬负责指导文章撰写以及最终定稿。
详细信息
    通信作者:

    宋冬, songdong@njmu.edu.cn (ORCID: 0009-0002-2432-2779)

Multiorgan crosstalk in the pathogenesis of hepatic encephalopathy

Research funding: 

2022 General Project of Philosophy and Social Science Research in Jiangsu Universities (2022SJYB1865);

2023 General Project of Education Research Topic of Nanjing Medical University (2023ZC104);

The Second Phase of ‘Scientific Research Talent Training Plan’ at Kangda College of Nanjing Medical University (KD2022KYRC012)

More Information
  • 摘要: 肝性脑病是肝硬化等终末期肝病常见且严重的并发症,其本质是由于急性或慢性肝功能严重障碍或门体分流引起的以代谢紊乱为基础的神经精神异常综合征。临床实践中,肝性脑病的发作与血氨水平并非完全线性相关,常由肝外因素诱发,提示其发病机制中存在多器官间的复杂交互。本文基于氨中毒、炎症、神经递质失衡及氧化/硝化应激4种主要发病机制,系统阐述肝性脑病中的多器官交互作用机制,并结合肌少症、糖尿病等新兴风险因素展开讨论,旨在为深入探究肝性脑病的病理生理机制及未来临床诊疗策略的制定提供新的理论依据。

     

  • 注: TNF-α,肿瘤坏死因子α;IL-6,白细胞介素6;ROS,活性氧;NADPH,还原型烟酰胺腺嘌呤二核苷酸磷酸。

    图  1  肝性脑病中的多器官交互作用机制

    Figure  1.  The mechanism of multiorgan crosstalk in hepatic encephalopathy

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出版历程
  • 收稿日期:  2025-10-14
  • 录用日期:  2025-10-27
  • 出版日期:  2026-05-20
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