Description
We found that PTC undergo polyploidization immediately after glycerol-induced rhabdomyolysis (nephrotoxic-AKI). Polyploidization of PTC is controlled by YAP1. Block of YAP1 related polyploidization of TC employing a specific inhibitor of YAP1 transcriptional activity (CA3) after the acute phase of damage prevented CKD progression after AKI. To identify novel pathways and potential targets involved in AKI response and subsequent CKD development, we generated single-cell RNA sequencing (scRNAseq) datasets from nephrotoxic-AKI female mice treated with vehicle or CA3 starting from 4 days after AKI. Mice were sacrificed two weeks after AKI, when blood urea nitrogen levels, that reflect kidney functionality, were found to start diverging between treated and control mice, but before CKD development.
Overall Design
To identify novel pathways and potential targets involved in the response to AKI and subsequent CKD development.
Curator
yq_pan