title: [Endothelium Aging and Oxidative Stress].
abstract: 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/Keapl-ARE, PPAR-y, SIRT and FOXO, etc. Among them, the Nrf2/Keapl-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 relationship between endothelial aging and oxidative stress may serve as a therapeutic clues in the treatment of oxidative stress-related diseases.
authors.forename: Bo
authors.initials: B
authors.lastname: Chen
authors.forename: Yan-Rong
authors.initials: YR
authors.lastname: Lu
authors.forename: You-Nan
authors.initials: YN
authors.lastname: Chen
authors.forename: Yu-Jian
authors.initials: YJ
authors.lastname: Kang
authors.forename: Jing-Qiu
authors.initials: JQ
authors.lastname: Cheng
mesh_terms: D000818:Animals; D016922:Cellular Senescence; D004194:Disease; D004730:Endothelium, Vascular / Q000378:metabolism / Q000503:physiopathology*; D006801:Humans; D008928:Mitochondria / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism*; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D017382:Reactive Oxygen Species / Q000378:metabolism; D015398:Signal Transduction
chemical_list: D017382:Reactive Oxygen Species; D052250:Nitric Oxide Synthase Type III