Provincial Key Laboratory for Developmental Biology and Neurosciences, Key Laboratory of Optoelectronic Science and Technology for Medicine of Ministry of Education, College of Life Sciences, Fujian Normal University, Fuzhou 350007, China.
Oxid Med Cell Longev. 2021 Oct 19;2021:6114132. doi: 10.1155/2021/6114132. eCollection 2021.
Hypoxia and oxidative stress are the common causes of various types of kidney injury. During recent years, the studies on hypoxia inducible factor- (HIF-) 1 attract more and more attention, which can not only mediate hypoxia adaptation but also contribute to profibrotic changes. Through analyzing related literatures, we found that oxidative stress can regulate the expression and activity of HIF-1 through some signaling molecules, such as prolyl hydroxylase domain-containing protein (PHD), PI-3K, and microRNA. And oxidative stress can take part in inflammation, epithelial-mesenchymal transition, and extracellular matrix deposition mediated by HIF-1 via interacting with classical NF-B and TGF- signaling pathways. Therefore, based on previous literatures, this review summarizes the contribution of oxidative stress to HIF-1-mediated profibrotic changes during the kidney damage, in order to further understand the role of oxidative stress in renal fibrosis.
缺氧和氧化应激是各种类型肾损伤的共同原因。近年来，缺氧诱导因子-1 (HIF-1) 的研究受到越来越多的关注，它不仅可以介导缺氧适应，还可以促进肾成纤维细胞的转化。通过分析相关文献，我们发现氧化应激可以通过脯氨酰羟化酶结构域蛋白（PHD）、PI-3K 和 microRNA 等信号分子调节 HIF-1 的表达和活性。氧化应激还可以通过与经典的 NF-κB 和 TGF-β信号通路相互作用，参与 HIF-1 介导的炎症、上皮间质转化和细胞外基质沉积。因此，基于以前的文献，本综述总结了氧化应激在肾脏损伤过程中对 HIF-1 介导的肾成纤维细胞转化中的作用，以进一步了解氧化应激在肾纤维化中的作用。
