干预CTGF在防治高血压早期肾损害肾脏纤维化中的价值  

Value of CTGF in the fight against early renal impairment renal fibrosis in high blood pressure patients

作　　者：王波[1] 戴小华[2] 

机构地区：[1]安徽中医学院,安徽合肥230038 [2]安徽省中医院心血管内科,安徽合肥230031

出　　处：《安徽医药》2011年第5期535-538,共4页Anhui Medical and Pharmaceutical Journal

基　　金：安徽省自然科学基金资助项目(No090413254)

摘　　要：近年发现,非血流动力学机制在高血压早期肾损害的发病过程中同样起着重要的作用。在非血流动力学诸多因素中,纤维化因子在高血压早期肾损害的发病过程中有着重要意义,其可导致肾脏纤维化(肾小球的硬化和肾小管的间质纤维化)。随着研究的深入,AngⅡ、TGFβ1、CTGF、血小板源生长因子、TNFα、ET-1、肝细胞生长因子、干扰素-γ等细胞因子及TβRⅠ、TβRⅡ、Sm ad2Sm ad3、Sm ad4、Sm ad7等参与成分作为评价肾脏纤维化的指标越来越被广泛的应用,它们之中究竟哪种更有前景?是实验和临床关注的重点?近年大量资料显示,AngⅡ、TGFβ1和CTGF在肾脏纤维化中的作用更为重要,可以作为评价高血压早期肾损害非血流动力学机制的较好指标。在它们之间,CTGF是AngⅡ-TGFβ1-TβR-Sm ads-CTGF通路的最终因子,可通过多靶点?多途径干预,同时只介导TGFβ1的负面效应,因此在防治高血压早期肾损害肾纤维化进程中有更为重要的价值。In recent years,it is found that non-hemodynamic mechanisms plays an important role in the pathogenesis of early renal damage in hypertensive patients.In many non-hemodynamic factors,fibrosis is significant in the pathogenesis of hypertensive renal damage,which can lead to renal fibrosis（glomerular sclerosis and tubular interstitial fibrosis）.With further research,Ang Ⅱ,TGFβ1,CTGF,platelet-derived growth factor,TNFα,ET-1,hepatocyte growth factor,interferon-γ and other cytokines and TβR Ⅰ,TβR Ⅱ,Smad2Smad3,Smad4,Smad7 are widely used as indicators to evaluate renal fibrosis.The recent data show that Ang Ⅱ,TGFβ1 and CTGF＇s role in renal fibrosis is more important,which can be used as better in dicators to evalscate early renal damage.Among them,CTGF is the final factor in Ang Ⅱ-TGFβ1-TβR-Smads-CTGF pathway through multi-target,multi-channel interference,while it only mediate the negative effect of TGFβ1,so it has more significant value in prevent early renal damage in hypertensive patients.

关 键 词：AngⅡ TGFΒ1 CTGF 

分 类 号：R544.1[医药卫生—心血管疾病]