AI Article Synopsis
- The study investigates the cellular processes involved in the recovery or fibrosis of kidneys following acute kidney injury (AKI) using single nucleus RNA sequencing in a mouse model.
- Researchers identified a specific state of proximal tubule cells that are proinflammatory and profibrotic, which is associated with unsuccessful repair after injury.
- The findings point to this failed-repair cell state (FR-PTC) as a potential target for therapies aimed at improving kidney recovery, as it is also observable in other injury models and human cases.
Article Abstract
After acute kidney injury (AKI), patients either recover or alternatively develop fibrosis and chronic kidney disease. Interactions between injured epithelia, stroma, and inflammatory cells determine whether kidneys repair or undergo fibrosis, but the molecular events that drive these processes are poorly understood. Here, we use single nucleus RNA sequencing of a mouse model of AKI to characterize cell states during repair from acute injury. We identify a distinct proinflammatory and profibrotic proximal tubule cell state that fails to repair. Deconvolution of bulk RNA-seq datasets indicates that this failed-repair proximal tubule cell (FR-PTC) state can be detected in other models of kidney injury, increasing during aging in rat kidney and over time in human kidney allografts. We also describe dynamic intercellular communication networks and discern transcriptional pathways driving successful vs. failed repair. Our study provides a detailed description of cellular responses after injury and suggests that the FR-PTC state may represent a therapeutic target to improve repair.
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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7355049 | PMC |
| http://dx.doi.org/10.1073/pnas.2005477117 | DOI Listing |
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