期刊文献+

以线粒体自噬为靶点的益气活血类中药保护心肌缺血再灌注损伤研究进展 被引量:3

Research progress on the protection of myocardial ischemia-reperfusion injury by Qi-enhancing and blood-activating traditional Chinese medicines targeting mitochondrial autophagy
下载PDF
导出
摘要 线粒体自噬是一种高度保守的线粒体降解过程。适当的线粒体自噬有利于维持心肌细胞内稳态,对保护缺血心肌具有重要意义。大量研究证实,中药单体、组分、复方可通过保护线粒体结构及功能,调节线粒体自噬,有效治疗缺血性心脏病。基于上述背景,本文以线粒体自噬为靶点,通过PINK1-Parkin、FUNDC1、BNIP3L/NIX等信号通路,对益气活血类中药提取物或复方在缺血性心脏病中的作用和机制进行综述,并结合实验室研究结果,为阐述益气活血类中药调控线粒体自噬的作用机制提供合理依据,以期为防治缺血性心脏病提供有效策略。 Mitochondrial autophagy is a highly conserved mitochondrial degradation process.Proper mitochondrial autophagy is beneficial to maintain homeostasis of cardiomyocytes and has important significance for protection of ischemic myocardium.A large number of studies have confirmed that TCM monomers,components and compounds can effectively treat ischemic heart disease by protecting mitochondrial structure and function,regulating mitochondrial autophagy.Based on the above background,this paper took mitochondrial autophagy as the target and reviewed the mechanisms of Qi-enhancing and blood-activating Chinese herbal extracts or compounds in ischemic heart disease through PINK1-Parkin,FUNDC1,BNIP3L/NIX and other signaling pathways.Combined with the results of our laboratory,in order to provide a reasonable basis for explaining the mechanism of regulating mitochondria autophagy by TCM of invigorating Qi and promoting blood circulation,and to provide effective strategies for preventing and treating ischemic heart disease.
作者 蔡丹阳 李洁 李运伦 CAI Danyang;LI Jie;LI Yunlun(The First Clinical College of Medicine,Shandong University of Traditional Chinese Medicine,Jinan 250355,China)
机构地区 山东中医药大学
出处 《环球中医药》 CAS 2023年第9期1913-1919,共7页 Global Traditional Chinese Medicine
基金 国家自然科学基金(82004277)。
关键词 缺血性心脏病 再灌注损伤 线粒体 线粒体自噬 益气活血类中药 中药提取物 信号通路 机制研究 Ischemic heart disease reperfusion injury mitochondria mitochondrial autophagy invigorating Qi and promoting blood traditional Chinese medicine extract signal path mechanism study
  • 相关文献

参考文献7

二级参考文献50

共引文献88

同被引文献38

引证文献3

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