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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 α  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- κ B and TGF- β  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.

Contribution of Oxidative Stress to HIF-1-Mediated Profibrotic Changes during the Kidney Damage