Gene Facilitating Repair Of Acutely Injured Kidney Found

In the kidney, injured cells can be kicked into reparative mode by a gene called Sox9, according to a new paper.  Sox9 also plays a key role in the normal development of the kidney and the authors found that surviving injured cells switch on the Sox9 gene as a response to kidney damage. This regenerates the injured cellular lining of the nephron, the functional unit of the kidney, and repairs the kidney after acute kidney injury (AKI).   By recruiting the majority of the surviving cells of the epithelium to aid in the timely repair of a severely injured organ, the kidney's Sox9 strategy contrasts with the stem cell-based repair strategy of many other organ systems.

In the kidney, injured cells can be kicked into reparative mode by a gene called Sox9, according to a new paper.  Sox9 also plays a key role in the normal development of the kidney and the authors found that surviving injured cells switch on the Sox9 gene as a response to kidney damage.

This regenerates the injured cellular lining of the nephron, the functional unit of the kidney, and repairs the kidney after acute kidney injury (AKI).  

By recruiting the majority of the surviving cells of the epithelium to aid in the timely repair of a severely injured organ, the kidney's Sox9 strategy contrasts with the stem cell-based repair strategy of many other organ systems.

In sections of the kidney that fail to repair, Sox9 remains activated thereby, demarcating regions of inefficient repair responses. Further interrogation of such regions could provide a crucial link between AKI and its transition to chronic and end-stage kidney disease.

"Currently, no treatment exists to treat AKI per se. Identifying the kidney's intrinsic mechanisms of repair is critical for developing treatments to kickstart the kidneys after AKI, a serious condition with an in-hospital mortality rate exceeding 50 percent," said first author Sanjeev Kumar, M.D., Ph.D., a Keck School of Medicine of University of Southern California postdoctoral research associate. 

Published in Cell Reports.
Source: University of Southern California - Health Sciences

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