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

作　　者：汪绪祥 王锁刚[2] WANG Xu-xiang;WANG Suo-gang(Master’s Degree 2017 of the First Clinical Medical College,Henan University of Chinese Medicine,Zhengzhou 450003,China;Department of Urology of the First Affiliated Hospital,Henan University of Chinese Medicine,Zhengzhou 450003,China)

机构地区：[1]河南中医药大学第一临床医学院,郑州450003 [2]河南中医药大学第一附属医院泌尿外科,郑州450003

出　　处：《南昌大学学报（医学版）》2020年第6期82-85,共4页Journal of Nanchang University：Medical Sciences

基　　金：河南省高等学校重点科研项目计划(19A360010)。

摘　　要：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.

关 键 词：慢性移植肾病 移植肾纤维化 TGFβ1-Smad/p38MAPK信号通路 机制 

分 类 号：R692[医药卫生—泌尿科学]