[关键词]
[摘要]
氧化应激(OS)是造成机体损伤的重要原因。既往研究显示缺血缺氧、过度光照以及高糖环境等多种因素均可引起视网膜活性氧和自由基增多，从而诱发OS，造成视网膜损伤并影响正常的视觉功能。Kelch样环氧氯丙烷相关蛋白1(KEAP1)与核因子E2相关因子2(NRF2)共同构成机体中主要的抗氧化应激信号通路，通过多种途径调节视网膜能量代谢及细胞增殖凋亡自噬等机制而发挥抗氧化作用，以减轻OS所致视网膜损伤。本文将简要综述视网膜中KEAP1-NRF2信号通路调控OS的作用及机制，以期为后续研究提供思路。
[Key word]
[Abstract]
Oxidative stress(OS)is a major reason for body damage. Studies have shown that a variety of factors, such as ischemia and hypoxia, excessive light and hyperglycemia can cause the increase of reactive oxygen species and free radicals in the retina, thus inducing OS, damaging retina and affecting the normal visual function. Kelch-like ECH-associated protein 1(KEAP1)and nuclear factor erythroid 2 related factor 2(NRF2), which together constitute the main antioxidant stress signaling pathway in the body, play an antioxidant role by regulating retinal energy metabolism and cell proliferation, apoptosis and autophagy through various ways, so as to reduce retinal damage caused by OS. In this paper, the role and mechanism of the KEAP1-NRF2 signaling pathway regulation of OS in the retinal are briefly reviewed, aiming to provide ideas for subsequent research.
[中图分类号]
[基金项目]
四川省科技厅自然基金面上项目(No.23NSFSC1940); 南充市市校科技战略合作项目(No. 22SXFWDF0003); 川北医学院附属医院项目(No. 2023ZD010)
