Abstract
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-1α 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-κB 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.
Highlights
The balance of oxygen consumption and supply is essential for all mammalian organs, providing fuel for various physiological metabolic processes and maintaining homeostasis [1]
It is demonstrated that acute kidney injury (AKI) and various chronic renal diseases (CKD) are associated with hypoxia and oxidative stress, which are more likely to develop into renal fibrosis eventually [3, 4]
Das et al found that the expression of NOX4 caused by Transforming growth factor- (TGF-)β activation can be reduced by blocking Smad2 or Smad3, which suggested that TGF-β/Smad2/3 upregulated NOX4 and induced reactive oxygen species (ROS) generation, such as H2O2, which played an important role in the progression of renal fibrosis [76,77,78]
Summary
The balance of oxygen consumption and supply is essential for all mammalian organs, providing fuel for various physiological metabolic processes and maintaining homeostasis [1]. It is demonstrated that acute kidney injury (AKI) and various chronic renal diseases (CKD) are associated with hypoxia and oxidative stress, which are more likely to develop into renal fibrosis eventually [3, 4]. We have reasons to believe that hypoxia and oxidative stress may play an important role in the destruction of renal tissue, irreversible loss of kidney function, and the progression of renal fibrosis [5, 6]. The present review is aimed at summarizing the profibrotic role and molecular regulation of HIF-1α on kidney damage, illustrating the interaction between HIF-1α and oxidative stress, and providing new insights for renal injury and aberrant tissue repair
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