Figure 1.

HIF-1α expression increases under hypoxia, which promoted renal fibrosis through the following aspects: Stimulating the secretion of interleukin-1β (IL-1 β) and tumor necrosis factor-α (TNF-α), and increasing the inflammatory reaction, upregulation of the epithelial cell marker E-cadherin and downregulation of the mesenchymal marker vimentin promote EMT, enhance pro-fibrosis cytokines such as plasminogen activator inhibitor 1 (PAI-1) and tissue inhibitor of metalloproteinase (TIMPs), and regulate fibrosis-related signaling pathways such as TGF-β/Smads signaling.