The Role of Sox9 in Kidney Repair After AKI
Dr. Sanjeev Kumar’s fellowship work explores the kidney’s ability to recover after acute kidney injury (AKI). AKI is characterized by a rapid decline in kidney function. It can be caused by major infections, trauma, or ischemia reperfusion injury (IRI), which occurs when the cells of the kidney are deprived of oxygen, often during cardiac surgery. An endogenous repair and regenerative process that restores the tubular epithelium and kidney function follows AKI. However, in patients where the repair process is inefficient, dialysis is required in the interim, to remove life-threatening toxic compounds. Despite advances in medical care, such patients continue to have high morbidity and mortality. Currently, no therapies exist to prevent or treat AKI and therefore, novel specific strategies are urgently required in an attempt to significantly improve the dismal outcome of this clinical syndrome.
One such strategy will be to harness the kidney’s prodigious capacity of intrinsic repair. However, little is known about the precise molecular responses that regulate tubular repair mechanisms. Better understanding of such mechanisms is imperative for the design of novel therapeutic strategies that could enhance tubular repair and kidney function post-AKI.
Dr. Kumar is currently examining the role of Sox9, a key kidney developmental gene, in kidney repair after AKI. The findings from this research study have the potential to identify and confirm Sox9 as an elusive bona fide marker that marks the dedifferentiation of the tubular cell upon injury to a “nephron progenitor or progenitor-like state”. In addition, the findings will also establish whether Sox9 per se contributes to repair processes in the mammalian kidney. Moreover, this study promises to identify, for the first time, gene regulatory networks that operate in solid organs after injury, thereby providing novel insights into the repair/regenerative process.