| Literature DB >> 35005326 |
Louisa M S Gerhardt1, Andrew P McMahon1.
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.Entities:
Keywords: ATAC sequencing; acute kidney injury; epigenomics; multi-omics; single-cell RNA-sequencing
Year: 2021 PMID： 35005326 PMCID： PMC8740908 DOI： 10.1016/j.cobme.2021.100344
Source DB: PubMed Journal: Curr Opin Biomed Eng ISSN： 2468-4511