SOX9 and acute kidney injury: In summary, hAD-MSC treatment promoted tubular repair and regeneration, through activating tubular Sox9, increasing the dedifferentiation and effective proliferation, improved cell cycle arrest and hypoxia, prevented the infiltration of inflammatory cells, which are the hallmarks for the transtion from AKI to CKD [37, 43], suggesting that hAD-MSCs had the potential to delay AKI and subsequent CKD.