TGF-β/Smad信号通路与心肌纤维化及蒽环类心脏毒性关系的研究进展  

Correlations of transforming growth factor-β/Smad signal pathway with myocardial fibrosis and anthracycline-induced cardiotoxicity

作　　者：尚娜 周毅[1] SHANG Na;ZHOU Yi(Department of Breast Surgery,the First Affiliated Hospital of Harbin Medical University,Harbin150001,China)

机构地区：[1]哈尔滨医科大学附属第一医院乳腺外科,哈尔滨150001

出　　处：《中华实用诊断与治疗杂志》2020年第5期527-530,共4页Journal of Chinese Practical Diagnosis and Therapy

基　　金：中国医药教育协会科研专项(药教协授字2016第128号)。

摘　　要：心肌纤维化是心肌重塑的主要表现之一,也是慢性心力衰竭发生的常见原因。转化生长因子-β(transforming growth factor-β,TGF-β)/Smad信号通路激活与心肌纤维化的发生、发展有关,而核转录共抑制因子SnoN可对TGF-β/Smad通路进行负调控。应用蛋白酶体抑制剂MG132阻断SnoN降解,上调SnoN蛋白表达,可拮抗TGF-β/Smad信号通路转导,减轻心肌纤维化。蒽环类化疗药物在乳腺癌化疗中具有重要作用,但其可导致心肌纤维化,造成心肌重塑甚至心力衰竭,临床应用受限。本文就TGF-β/Smad信号通路、SnoN蛋白在TGF-β/Smad信号通路中的作用、MG132对心肌纤维化的治疗作用以及TGF-β/Smad信号通路与蒽环类化疗药物心脏毒性关系的研究进展作一综述。Myocardial fibrosis is not only one of the main manifestations of myocardial remodeling,but also the cause of chronic heart failure.The activation of transforming growth factor-β(TGF-β)/Smad signal pathway can lead to the occurrence and development of myocardial fibrosis,while SnoN can negatively regulate the TGF-β/Smad pathway.Proteasome inhibitor MG132can be used to block the degradation of SnoN,increase the level of SnoN protein,antagonize TGF-β/Smad signal transduction,and inhibit the occurrence and development of myocardial fibrosis.Despite the important effect of anthracycline on breast cancer,it would induce myocardial fibrosis,myocardial remodeling and even heart failure,therefore it is limited in clinical application.This paper reviews the research progress of TGF-β/Smad signal pathway,the role of SnoN protein in TGF-β/Smad signal pathway,the therapeutic effect of MG132on myocardial fibrosis,and the relationship between TGF-β/Smad signal pathway and anthracycline-induced cardiotoxicity.

关 键 词：乳腺癌 心肌纤维化 转化生长因子-β/Smad信号通路 SNON MG132 蒽环类化疗药物 

分 类 号：R542.23[医药卫生—心血管疾病]