Hypoxia Triggers Signatures of Maladaptive Repair in Human Kidney Organoids [bulk RNA-seq]

Chronic kidney disease (CKD) affects over half of all adults over 70 and 13% of the global population. The development of renal fibrosis is strongly correlated with loss of kidney function during CKD and involves cellular injury, excessive production of extracellular matrix proteins and inflammation. Current treatments focus on controlling blood pressure, controlling diabetes, and steroid therapies; however, we have no treatments to suppress renal fibrosis. Because hypoxia plays a key role in the development and progression of CKD, we have developed a new model of induced pluripotent stem cell-derived kidney organoids to study in vitro the development of fibrosis in a human model. Eighteen-day old kidney organoids are exposed to hypoxic conditions (1% O2) for 48h. To assess the development of maladaptive repair following acute injury, kidney organoids are afterwards placed back into normoxic conditions (21% O2) for an extra 5 days. Comparative gene expression profiling analysis of bulk RNA-seq data of kidney organoids on day 20 and day 25 of development for both injury and control groups.