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Probing the Molecular Events Linking Kidney Injury to Fibrosis

New research has utilized cutting-edge methods to analyze the way different types of cells respond to kidney injuries that lead to fibrosis in two mouse models of kidney injury. Acute kidney injury (AKI) often leads to chronic kidney disease—and sometimes to kidney failure—by triggering events that lead to kidney fibrosis, or scarring. Clarifying the molecular links between injury and fibrosis in the kidney might therefore suggest new and better ways to treat people with AKI to prevent long-term kidney damage.

To identify the processes involved, scientists used male mice in which one kidney was injured either by a temporary blockage of blood flow or by a temporary block of the path for urine to drain from the kidney. Using 24 kidneys from mice with one injury type or the other, they used high-throughput methods that allowed them to record details of genetic activity in over 300,000 cells, including 50 different cell types. These experiments revealed a wide variety of cellular responses in the different types of kidney injury. The animals with AKI caused by blood flow restriction were more likely to recover their kidney function than those with AKI from temporary urinary obstruction, and researchers found differences in genetic activity in various cell types that might help explain the unequal outcomes. Comparing these changes to cellular responses from other mouse models as well as human kidney disease states allowed the researchers to verify that many were relevant to human disease. Study scientists assembled their data into an atlas of genetic activity profiles of various cell types from the two injury states, which is available on the web as a useful resource for future research. This atlas is improving our understanding of the pathways that lead to kidney fibrosis and could one day lead to treatments that help prevent chronic kidney disease from developing in people who experience AKI.

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