期刊文献+

基于TGF-β1/Smads信号通路治疗心肌梗死后心肌纤维化的研究进展 被引量:35

The research progress on treatment of myocardial fibrosis by regulating TGF-β1/Smads pathway
暂未订购
导出
摘要 心肌梗死后心肌纤维化是心脏重塑从而导致心脏衰竭的重要原因,造成心肌梗死后心室重构的机制复杂,是多因素相互作用、共同参与的结果。但其中机制较为明确,并且在心肌纤维化进程中扮演重要作用的是TGF-β1依赖的Smads信号通路。心肌梗死后,活化的TGF-β1可以通过下游Smads信号发挥持续的生物学效应,活化成纤维细胞,引起细胞外基质沉积,使心肌成纤维细胞向肌成纤维细胞分化。因此,如何阻抑或控制TGF-β1/Smads信号通路是治疗心肌梗死后心肌纤维化的重要研究方向,该文就当前基于TGF-β1/Smads信号通路治疗心肌梗死后心肌纤维化的研究进行综述。 Myocardial fibrosis leads to cardiac remodeling and heart failure after myocardial infarction. The mechanism of ventricular remodeling after myocardial infarction is complicated,which results from multi-factor interactions. TGF-β1-dependent Smads signal pathway is a definite mechanism which plays an important role in the process of myocardial fibrosis. Myocardial infarction activates the TGF-β1,which links the downstream Smads signaling to play a sustained biological effects via the accumulation of activated cardiac fibroblasts and excess deposition of extracellular matrix,and the differentiation from myocardial fibroblasts to myofibroblasts. Therefore,how to block or control TGF-β1/Smads signaling pathway is an important research direction for the treatment of myocardial fibrosis after myocardial infarction. This paper reviews the current studies of the treatment of myocardial fibrosis after myocardial infarction based on the TGF-β1/Smads signaling pathway.
出处 《中国药理学通报》 CAS CSCD 北大核心 2018年第1期5-8,共4页 Chinese Pharmacological Bulletin
基金 国家中医临床研究基地业务建设科研专项课题(No JDZX2015006)
关键词 心肌梗死 心肌纤维化 TGF-Β/SMADS TGF-Β1 治疗靶点 治疗进展 myocardial infarction myocardial fibrosis TGF-β/Smads TGF-β1 Smad2/3 therapeutic target therapeutic progress
  • 相关文献

参考文献3

二级参考文献21

  • 1吴以岭,谷春华,徐贵成,魏聪,高学东.芪苈强心胶囊治疗慢性心力衰竭随机双盲、多中心临床研究[J].疑难病杂志,2007,6(5):263-266. 被引量:88
  • 2Segura A M, Frazier O H, Buja L M. Fibrosis and heart failure [J]. Heart Fail Rev,2014,19(2):173.
  • 3Porter K E, Turner N A. Cardiac fibrablasts : at the heart of myo- cardial remodeling[ J ]. Pharmacol Ther,2009, 123 (2) :255.
  • 4Yuan S M, Jing H. Cardiac pathologies in relation to Smad-de- pendent pathways [ J ]. Interact Cardiovasc Thorac Surg, 2010,11 (4) : 455.
  • 5E1-Sheakh A R, Ghoneim H A, Suddek G M. Attenuation of oxi- dative stress, inflammation, and endothelial dysfunction in hyper- cholesterolemic rabbits by allicin[ J]. Can J Physiol Pharmacol, 2015, 14:1.
  • 6Kaga S, Zhan L, Matsumoto M, et al. Resveratrol enhances neo- vaseularization in the infarcted rat myocardium through the indue-tion of thioredoxin-1, heme oxygenase-1 and vascular endothelial growth factor[ J]. J Mol Cell Cardiol, 2005, 39:813.
  • 7Penumathsa S V, Thirunavukkarasu M, Koneru S, et al. Statin and resveratrol in combination induces cardioprotection against myocardial infarction in hypercholesterolemic rat [ J ]. J Mol Cell Cardiol, 2007, 42:508.
  • 8Rogers T B, Pati S, Gaa S, et al. Mesenchymal stem cells stimu- late protective genetic reprogramming of injured cardiac ventricu- lar myocytes[ J]. J Mol Cell Cardiol,2011,50 :346.
  • 9Watanabe K, Sukumaran V, Veeraveedu P T, et al. Regulation of inflammation and myocardial fibrosis in experimental autoim- mune myocarditis[J]. Inflamm Allergy Drug Targets,2011,10: 218.
  • 10Wang S L, Liu D S, Liang E S, et al. Protective effect of allicin on high glucose/hypoxia-induced aortic endothelial ceils via re- duction of oxidative stress [ J]. Exp Ther Med, 2015, 10 (4) : 1394.

共引文献78

同被引文献384

引证文献35

二级引证文献225

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部