驱动肾小管间质纤维化的新机制

Novel mechanisms driving renal tubulointerstitial fibrosis

肾纤维化,尤其是肾小管间质纤维化,是所有慢性肾脏疾病进展为终末期肾病的最常见途径。肾小管上皮细胞在受到慢性损伤后会发生糖脂代谢改变、未折叠蛋白反应、自噬和衰老、上皮细胞-间充质转化和细胞周期G2/M期停滞等几种适应性反应。修复机制适应不良,会诱导产生肾小管间质纤维化。本文将讨论肾小管上皮细胞的这些适应性反应驱动肾小管间质纤维化的分子机制,为探寻肾小管间质纤维化新的药物作用靶点提供参考。

Renal fibrosis,especially tubulointerstitial 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,epithelial-to-mesenchymal transition and G2/M cell cycle arrest.Maladaptive repair mechanisms can induce tubulointerstitial fibrosis.This article will discuss the molecular mechanism of these adaptive responses of renal tubular epithelial cells driving renal tubulointerstitial fibrosis,and provide a basis for exploring new drug targets for renal tubulointerstitial fibrosis.