Renal fibrosis,especially tubulointer-stitial fibrosis,is the most common pathway of all chronic kidney diseases progressing to end-stage renal diseases.Several adaptive reactions occur in renal tubular epithelial cells after chronic injury,such as changes in glycolipid metabolism,unfolded protein response,autophagy and senescence,epi-thelial-to-mesenchymal transition and G2/M cell cy-cle arrest.Maladaptive repair mechanisms can in-duce tubulointerstitial fibrosis.This article will dis-cuss the molecular mechanism of these adaptive responses of renal tubular epithelial cells driving re-nal tubulointerstitial fibrosis,and provide a basis for exploring new drug targets for renal tubulointer-stitial fibrosis.