移植肾纤维化与TGFβ1-Smad/p38MAPK信号通路的研究进展

Research Progress in Transplanted Kidney Fibrosis and TGFβ1-Smad/p38MAPK Signaling Pathway

慢性移植肾病(CAN)是移植肾远期失去功能或者功能不全的首要原因,严重影响了异体肾移植受者的生活质量和长期存活,而移植肾纤维化是CAN病理改变的核心。TGFβ1-Smad/p38MAPK信号传导途径可以介导肾小管上皮-间质转分化的全过程。如何预防和减缓移植肾纤维化进展至CAN仍是世界性的难题。文章总结了移植肾纤维化与TGFβ1-Smad/p38MAPK信号通路的关系以及防治CAN的理论和实验依据。

Chronic allograft nephropathy(CAN),a leading cause of long-term loss of function or dysfunction in transplanted kidneys,seriously affects the quality of life and long-term survival of allogeneic kidney transplant recipients.Transplanted renal fibrosis is the core of pathological changes in CAN.The TGFβ1-Smad/p38MAPK signaling pathway mediates the whole process of renal tubular epithelial-mesenchymal transition.How to prevent and slow the progression of transplanted renal fibrosis to CAN is still a worldwide problem.This article reviews the relationship between transplanted renal fibrosis and TGFβ1-Smad/p38MAPK signaling pathway and summarizes theoretical and experimental basis for the prevention and treatment of CAN.