GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE99nnn/GSE99325/primaryOK2000000GenomicsHomo sapiensExpression profiling by arrayhttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE99325GEOGSE0falseTranscriptome-based network analysis reveals renal cell type-specific dysregulation of hypoxia-associated transcripts [Tub-FE]Accumulating evidence suggests that dysregulation of hypoxia-regulated transcriptional mechanisms is involved in development of chronic kidney diseases (CKD). However, it remains unclear how hypoxia-induced transcription factors (HIFs) and subsequent biological processes contribute to CKD development and progression. In our study, genome-wide expression profiles of more than 200 renal biopsies from patients with different CKD stages revealed significant correlation of HIF-target genes with eGFR in glomeruli and tubulointerstitium. These correlations were positive and negative and in part compartment-specific. Microarrays of proximal tubular cells and podocytes with stable HIF1α and/or HIF2α suppression displayed cell type-specific HIF1/HIF2-dependencies as well as dysregulation of several pathways. WGCNA analysis identified gene sets that were highly coregulated within modules. Characterization of the modules revealed common as well as cell group- and condition-specific pathways, GO-Terms and transcription factors. Gene expression analysis of the hypoxia-interconnected pathways in patients with different CKD stages revealed an increased dysregulation with loss of renal function. In conclusion, our data clearly point to a compartment- and cell type-specific dysregulation of hypoxia-associated gene transcripts and might help to improve the understanding of hypoxia, HIF dysregulation, and transcriptional program response in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 sapiens[28819298]