PI3K/Akt/mTOR通路与自噬在类风湿关节炎滑膜细胞增生中的意义

被引：32

作者：

孟明

梁红格

方皓

周蕾

冯建勇

董阳

闫振

陈冬志

机构：

[1] 河北大学基础医学院

来源：

医学研究与教育 | 2013年 / 05期

关键词：

自噬; Ⅱ型细胞凋亡; P13K/Akt/mTOR; RASF; 血小板活化颗粒;

D O I：

暂无

中图分类号：

R593.22 [类风湿性关节炎];

学科分类号：

100201 [内科学];

摘要：

细胞自噬是生物体生长发育中极为关键的自救行为,在应激状态下,通过清除细胞内变性蛋白及坏死物质,重建结构,维持细胞生存,但过度的自噬则会引起细胞的Ⅱ型凋亡。PI3K/Akt/mTOR是广泛存在于多种细胞内的一条重要信号通路,参与体内多种生理病理过程,其活化后对细胞自噬有抑制作用。在类风湿关节炎发病的早期,滑膜成纤维细胞(RASF)可通过多种途径启动自噬,维持RASF细胞内环境的稳定和细胞增生,随着病情的进展,血小板活化颗粒如PDGFRα等释放后可通过激活RASF中的PI3K/Akt/mTOR信号通路抑制自噬,从而避免RASF因过度自噬而诱导的Ⅱ型细胞凋亡,使滑膜细胞持续增生,加重RA的病情。本文旨在对PI3K/Akt/mTOR信号通路与自噬影响RA滑膜细胞持续增生的意义进行综述,以期探讨RA的发病机制、寻找新的治疗靶点。

引用

页码：69 / 74

页数：6

共 18 条

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