Abstract: Acute kidney injury(AKI)is an increasingly common complication during hospitalization with high morbidity and mortality.In recent years,it has been found that AKI is an independent risk factor for chronic kidney disease(CKD).Studies show that oxidative stress,endoplasmic reticulum stress,macrophage polarization and tubule cell cycle arrest are all involved in the pathophysiological process of progression from AKI to CKD.Increasing evidence suggests that renal tubular epithelial cell cycle arrest may play an important role in the progression of fibrosis.Indeed,during the maladaptive repair after a renal injury,many tubular cells that are undergoing cell division spend a prolonged period in the G2/M phase of the cell cycle.This article reviews the maladaptive repair after AKI,which is mainly caused by G2/M cell cycle arrest and the related factors involved in the regulation of G2/M arrest,leading to the development of progressive renal fibrosis.