Multi-omic approaches to acute kidney injury and repair

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 proinflammatory senescent molecular signature. Epigenetic studies have highlighted dynamic changes in the chromatin landscape of the kidney following AKI and have 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.

Automated summary

The kidney has a strong regenerative capacity, but severe acute kidney injury (AKI) or recurrent injuries can lead to chronic kidney disease (CKD) progression. Single-cell and epigenetic studies have provided insights into cell states and transcription factors following AKI.