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Updated: Oct 7, 2025

Bilateral Renal Ischemia-Reperfusion Model for Acute Kidney Injury in Mice
Published on: February 2, 2024
Multi-omic approaches to acute kidney injury and repair
Louisa M S Gerhardt1, Andrew P McMahon1
1Department of Stem Cell Biology and Regenerative Medicine, Eli and Edythe Broad Center for Regenerative Medicine and Stem Cell Research, Keck School of Medicine of the University of Southern California, Los Angeles, CA 90033, USA.
Abstract:
The kidney has a remarkable regenerative capacity. In response to ischemic or toxic injury, proximal tubule cells can proliferate to rebuild damaged tubules and restore kidney function. However, severe acute kidney injury (AKI) or recurrent AKI events can lead to maladaptive repair and disease progression from AKI to chronic kidney disease (CKD). The application of single cell technologies has identified injured proximal tubule cell states weeks after AKI, distinguished by a pro-inflammatory senescent molecular signature. Epigenetic studies highlighted dynamic changes in the chromatin landscape of the kidney following AKI and described key transcription factors linked to the AKI response. The integration of multi-omic technologies opens new possibilities to improve our understanding of AKI and the driving forces behind the AKI-to-CKD transition, with the ultimate goal of designing tailored diagnostic and therapeutic strategies to improve AKI outcomes and prevent kidney disease progression.
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