Abstract:

The most common cause of acute kidney injury (AKI) is apoptosis or necrosis of proximal tubular epithelial cells.Injury induces activation of key developmental transcription factors,activates the intrinsic molecular driver of epithelial regeneration,and promotes nephron epithelialmesenchymal transition.Complex molecular interactions between renal tubular epithelial cells and immune,interstitial and endothelial cells regulate renal repair.Unlike the commonly recognized proinflammatory and profibrotic effects,more and more studies have indicated the presence of macrophages,Tcell,and Bcell subtypes that promote renal recovery after injury.Regions of mild to moderate acute nephron injury,the injured nephron epithelial cells regenerate and completely repair to the previous morphology.In areas with severe injury,the regeneration process is subject to loss,resulting in extensive tissue remodeling and fibrosis.

Key words: acute kidney injury, renal repair, tubular epithelial cells, molecular mechanism