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陈晨, 殷园园, 武夏芳, 武瑞瑞, 徐苑苑. 活性氧通过MAPKs和PI3K/AKT通路激活Nrf2研究进展[J]. 中国公共卫生, 2016, 32(6): 870-873. DOI: 10.11847/zgggws2016-32-06-41
引用本文: 陈晨, 殷园园, 武夏芳, 武瑞瑞, 徐苑苑. 活性氧通过MAPKs和PI3K/AKT通路激活Nrf2研究进展[J]. 中国公共卫生, 2016, 32(6): 870-873. DOI: 10.11847/zgggws2016-32-06-41
CHEN Chen, YIN Yuan-yuan, WU Xia-fang.et al, . Advance in researches on role of MAPK and PI3K/AKT pathways in ROS-induced activation of nuclear factor erythroid 2-related factor 2[J]. Chinese Journal of Public Health, 2016, 32(6): 870-873. DOI: 10.11847/zgggws2016-32-06-41
Citation: CHEN Chen, YIN Yuan-yuan, WU Xia-fang.et al, . Advance in researches on role of MAPK and PI3K/AKT pathways in ROS-induced activation of nuclear factor erythroid 2-related factor 2[J]. Chinese Journal of Public Health, 2016, 32(6): 870-873. DOI: 10.11847/zgggws2016-32-06-41

活性氧通过MAPKs和PI3K/AKT通路激活Nrf2研究进展

Advance in researches on role of MAPK and PI3K/AKT pathways in ROS-induced activation of nuclear factor erythroid 2-related factor 2

  • 摘要: 机体在应对过量活性氧(ROS)时能够通过一些细胞信号转导通路,增强细胞内许多保护性蛋白的表达。核因子E2相关因子 2(Nrf2)是细胞对抗氧化应激的重要调控因子之一,在ROS诱导的抗氧化蛋白表达中具有重要作用。然而ROS激活Nrf2的具体机制并不完全清楚。有研究表明ROS可通过丝裂原活化的蛋白激酶(MAPKs)和磷脂酰肌醇-3-激酶/蛋白激酶B(PI3K/AKT)细胞信号通路激活Nrf2,以应对氧化应激对细胞造成的损伤。提示,MAPKs、PI3K/AKT 2个重要的信号通路在ROS诱导的Nrf2活化中具有重要作用。

     

    Abstract: When exposed to excessive reactive oxygen species (ROS),living organism can enhance the expression of many protective proteins through activation of a series of complex cellular signal transductions.Nuclear factor erythroid 2-related factor 2 (Nrf2) is a master transcription factor in cellular defense against oxidative stress,which is the key to ROS-induced overexpression of antioxidant proteins.Nevertheless,the mechanisms,by which ROS activate Nrf2,are not completely understood.Some researches show that ROS can activate Nrf2 through mitogen-activated protein kinases (MAPKs) and phosphatidylinositol-3-kinase/protein kinase B (PI3K/AKT) pathways,protecting cells from oxidative stress.It indicates that MAPKs and PI3K/AKT pathways play an important role in ROS-meditated activation of Nrf2.

     

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