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. Author manuscript; available in PMC: 2024 Dec 20.
Published in final edited form as: Nat Rev Nephrol. 2024 Apr 17;20(7):447–459. doi: 10.1038/s41581-024-00834-0

Fig. 1. Induction of cell states in the kidney tubule following AKI.

Fig. 1

The schematic illustrates a general model of the involvement of tubular epithelial cell states in AKI. This includes the emergence of distinct AKI-induced epithelial cell states, labeled by different colors. An unknown population of injured dedifferentiated epithelial cells undergoes cell cycling and replaces neighboring cells that have been lost. While some injured epithelial cells are able to regenerate and restore normal kidney epithelium through adaptive repair, a subset of dedifferentiated epithelial cells may persist in an aberrant cell state, contributing to chronic injury through a pro-inflammatory secretory phenotype. This further attracts immune cells and potentially causes harm to adjacent healthy kidney epithelium. It is important to note that this figure represents a single time point after AKI, where multiple AKI-induced cell states coexist. It should be noted that the presence and abundance of these cell states may vary between individuals and within any individual depending on the time point after AKI. It is of note that these mechanisms not restricted to the PT.