CAJ | 학술논문

内皮活性氧主要来源于线粒体、内皮一氧化氮合成酶和 NADPH 氧化酶4。过量活性氧是氧化应激的主要原因，也是内皮衰老及相关疾病的主要原因之一。但细胞已经进化出合适的抗氧化信号通路及时清除过量活性氧，如 Nrf2／Keap1-ARE、PPARγ、SIRT 和 FOXO 等。其中，Nrf2／Keap1-ARE 信号通路是目前已知的最强大内源性抗氧化信号通路。而且，这些通路之间可以协同作用抵抗氧应激损伤并促进细胞存活。对内皮衰老和氧化应激之间的关系理解有助于提供防治氧化应激相关疾病有用信息。
내피활성양주요래원우선립체、내피일양화담합성매화 NADPH 양화매4。과량활성양시양화응격적주요원인，야시내피쇠로급상관질병적주요원인지일。단세포이경진화출합괄적항양화신호통로급시청제과량활성양，여 Nrf2／Keap1-ARE、PPARγ、SIRT 화 FOXO 등。기중，Nrf2／Keap1-ARE 신호통로시목전이지적최강대내원성항양화신호통로。이차，저사통로지간가이협동작용저항양응격손상병촉진세포존활。대내피쇠로화양화응격지간적관계리해유조우제공방치양화응격상관질병유용신식。
In the endothelium,ROS mainly derive from mitochondria,endothelial nitric oxide synthases and NADPH oxidases 4.Excessive ROS are a major cause of oxidative stress,the primary stimulus of vascular dysfunction and oxidative stress-related diseases.However,cellular evolution has made possible the development of adaptive antioxidant systems that scavenge excessive ROS,such as Nrf2 /Keap1 -ARE, PPARγ,SIRT and FOXO,etc.Among them,the Nrf2 /Keap1 -ARE signaling pathway is perhaps the most prominent.What is more,there are the "crosstalk"among these antioxidant stress-related signaling pathways aim to alleviate oxidative stress injurys and promote cells survival.The understanding of the re-lationship between endothelial aging and oxidative stress may serve as a therapeutic clues in the treatment of oxidative stress-related diseases.