Conversely, during hypoxia HIF1α is not hydroxylated, which results in increased net levels of HIF1α and subsequent activation of HIF1α target gene expression, such as transforming growth factor-β (TGF-β), connective tissue growth factor (CTGF) and vascular endothelial growth factor (VEGF), and plays a critical role in glomerulosclerosis and renal fibrosis in CKD (19). This evidence concerns the gene HIF1A and glomerulosclerosis.