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急性胰腺炎胰酶异常活化和分泌的分子机制

崔恬玉 刘瑞霞 阴赪宏

引用本文:
Citation:

急性胰腺炎胰酶异常活化和分泌的分子机制

DOI: 10.3969/j.issn.1001-5256.2022.05.047
基金项目: 

北京市教育委员会科技计划一般项目 (KM201910025007);

国家自然科学基金 (81571933)

利益冲突声明:所有作者均声明不存在利益冲突。
作者贡献声明:崔恬玉负责拟定写作思路,检索文献,撰写论文; 刘瑞霞、阴赪宏负责指导、修改论文并最终定稿。
详细信息
    通信作者:

    阴赪宏,yinchh@ccmu.edu.cn

Research advances in abnormal activation and secretion of pancreatic enzymes in acute pancreatitis

Research funding: 

Beijing Municipal Commission of Education (KM201910025007);

National Natural Science Foundation of China (81571933)

More Information
  • 摘要: 胰腺腺泡细胞内胰酶异常活化和分泌是急性胰腺炎(AP)的重要发病机制之一,可直接损伤胰腺组织加速疾病进程,诱发重症急性胰腺炎。目前临床抑制胰酶异常活化和分泌的药物效果欠佳,探寻新的治疗靶点十分重要。本文归纳了AP胰酶异常活化和分泌的病理事件(胞浆钙离子超载、溶酶体与酶原颗粒的共定位、细胞器损伤、胰酶顶端侧分泌受阻和基底侧分泌增加等),搜集了相关事件的分子机制,讨论了胰酶异常活化和分泌在AP早期的作用过程,为未来靶向药物的研发提供思路。

     

  • 图  1  VAMP8介导的顶端侧分泌受损和基底侧分泌增强示意图

    Figure  1.  Schematic illustration of VAMP8-mediated impaired apical secretion and enhanced basal secretion

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  • 收稿日期:  2021-08-31
  • 录用日期:  2021-10-08
  • 出版日期:  2022-05-20
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