ROS调节mTOR信号通路参与自噬的研究进展  被引量:13

Research progress of ROS regulated mTOR signaling pathway involved in autophagy

在线阅读下载全文

作  者:张军[1,2] 谷翔[1] 黄问银[1] 张普华[1] 殷嫦嫦[3] ZHANG Jun GU Xiang HUANG Wenyin YING Changchang(Department the Affiliated Hospital of Jiujiang University, Jiujang, Jiangxi, 332000, China Medicine Graduate School, Nanchang University, Nanchang, 330006, China Basic Medical College of Jiujiang University)

机构地区:[1]九江学院附属医院心内科,江西九江332000 [2]南昌大学研究生院医学部,南昌330006 [3]九江学院基础医学院

出  处:《临床心血管病杂志》2016年第12期1266-1270,共5页Journal of Clinical Cardiology

摘  要:自噬是真核细胞中普遍存在的一种物质降解途径,通过自噬溶酶体介导,清除自身多余或受损的细胞器,参与正常细胞内稳态的维护,对机体生长、发育和衰老均起重要作用。哺乳动物雷帕霉素靶蛋白(mTOR)是一种丝/苏氨酸蛋白质激酶,接受并整合细胞内外的各种信号,是调节蛋白质翻译与细胞生长等多种生理活动的中心信号分子。而活性氧类(ROS)作为第2信使分子,可介导多种细胞信号通路并发挥广泛的生理效应。研究发现,在自噬的过程中,ROS可通过一定的途径激活或抑制mTOR通路,但其调节机制极其复杂。本文就自噬过程中ROS与mTOR之间相互调节机制的研究进展进行综述。Autophagy, a kind of material degradation pathway mediated by autophagy-lysosome in eukaryotic cells,can remove their excess or damaged organelles and to maintain intracellular material recycling and regulate homeostasis. It plays an important role in the body's growth, development and aging. Mammals rapamycin target protein (mTOR) is a kind of silk/threonine protein kinase, accepting and integrating signals inside and outside cells, which is center signal molecules of regulating protein translation, the cell growth and a variety of physiological activity. Reactive oxygen species (ROS) as the second messenger molecules mediate many kinds of cell signaling pathways and play a wide range of physiological effects. The study found that ROS can involve in the process of autophagy via activating or inhibiting mTOR pathways. However, the regulating mechanism is especially intricate. The article will discuss the research progress of the regulation mechanism between ROS and mTOR in the autophagy process.

关 键 词:活性氧类 哺乳动物雷帕霉素靶蛋白 自噬 

分 类 号:R34[医药卫生—基础医学]

 

参考文献:

正在载入数据...

 

二级参考文献:

正在载入数据...

 

耦合文献:

正在载入数据...

 

引证文献:

正在载入数据...

 

二级引证文献:

正在载入数据...

 

同被引文献:

正在载入数据...

 

相关期刊文献:

正在载入数据...

相关的主题
相关的作者对象
相关的机构对象