Welcome to the Mouse Kidney IRI Atlas

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).