内质网应激在肝衰竭发病机制中的作用

张向颖; 任锋

doi:10.3969/j.issn.1001-5256.2019.09.006

内质网应激在肝衰竭发病机制中的作用

DOI: 10.3969/j.issn.1001-5256.2019.09.006

张向颖,
任锋

首都医科大学附属北京佑安医院肝病研究所

详细信息

中图分类号: R575.3
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出版历程
- 收稿日期: 2019-06-03
- 出版日期: 2019-09-20

Role of endoplasmic reticulum stress in the pathogenesis of liver failure

Institute of Hepatology, Beijing YouAn Hospital, Capital Medical University

摘要

摘要: 肝衰竭的病理过程复杂,病情进展迅速,病死率高,需对其发病机制进行深入研究。早期的,轻度的内质网应激(ERS)可以通过未折叠蛋白反应维持细胞内环境稳定,而持续的、严重的ERS会促进炎症反应及细胞凋亡引起细胞死亡,因此ERS在疾病的发生发展过程中发挥关键作用。主要阐述ERS及其相关信号通路在肝衰竭发病机制中的作用,为肝衰竭的治疗提供新思路。
- 内质网应激 /
- 肝功能衰竭 /
- 细胞凋亡 /
- 炎症 /
- 未折叠蛋白反应
Abstract: Liver failure is a severe liver disease with a complex pathological process, rapid disease progression, and a high mortality rate, and in-depth studies are needed to explore its pathogenesis. Early and mild endoplasmic reticulum stress ( ERS) can maintain the stability of intracellular environment through unfolded protein reaction, while persistent and severe ERS may promote inflammatory response and apoptosis and cause cell death, and therefore, ERS plays a key role in the development and progression of liver failure. This article elaborates on the role of ERS and related signaling pathways in the pathogenesis of liver failure, so as to provides new ideas for the treatment of liver failure.
- endoplasmic reticulum stress /
- liver failure /
- apoptosis /
- inflammation /
- unfolded protein response

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参考文献(43)

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