The kidney tubules have tremendous capacity to regenerate following acute kidney injury (AKI) and most cases resolve via adaptive regeneration, however, in some patients AKI leads to long-term fibrosis and chronic kidney disease (CKD). A key bottleneck in the understanding of adaptive and maladaptive regeneration has been the limited insight into temporal and cell-specific genome-wide gene expression changes to define signals that initiate and drive cell differentiation and cell-cell interactions.

Here, we developed a model of adaptive and fibrotic kidney regeneration by titrating ischemic injury dose (short vs. long). We profiled transcriptomic changes at single-cell level (>110,000 cells) over time (1, 3, and 14 days post-ischemia).