Gene expression signatures of polyploid RTECs post-IRI

Acute kidney injury (AKI) is associated with high morbidity and mortality and is recognized as a common risk factor for chronic kidney disease (CKD). The role of renal tubular epithelial cell (RTEC) polyploidization in the AKI-to-CKD transition is well documented, while the underlying regulatory and molecular mechanisms remain poorly understood. To identify the phenotype switching and function variation in polyploid RTECs post-AKI, we performed RNA-sequencing analysis of different ploidy RTECs from the kidney of ischemia-reperfusion injury (IRI)-3-day mice.