摘要
缺血性心肌损伤的分子病理机制一直备受国际关注。该文应用C57BL/6品系的野生型(WT)小鼠、极低密度脂蛋白(Very Low Density Lipoprotein,VLDL)受体基因敲除(VLDLR-KO)小鼠、心脏特异性转基因(VLDLR-TG)小鼠,通过在体及离体实验研究VLDL受体对小鼠缺血性心肌损伤的影响,构建生物分子网络研究VLDL受体发挥生物学功能的关键分子及其关键信号通路。通过生物网络的功能模块计算,发现了VLDL受体→MAPKs、AKT、NF-κB信号通路→心肌损伤病理表型的因果关联性,阐明了VLDL受体影响缺血性心肌损伤的分子机制。
The molecular mechanism of ischemic myocardial injury is still a hot topic in the international academic circles.In this paper,C57 BL/6 wild type（WT） mouse strains,very low density lipoprotein（VLDL） receptor knockout（VLDLR-KO） mice and VLDL receptor transgenic（VLDLR-TG） mice,were selected to investigate on the effect of VLDL receptor on myocardial ischemic injury in vivo and in vitro.Key molecular signaling pathways were found based on the biomolecular network analyses.A causal relationship between VLDL receptor→MAPKs,AKT,NF-κB signaling pathway and the pathological phenotype of myocardial infarction,was identified by computational analysis of functional modules across biological networks,to illustrate the effect of VLDL receptor molecular mechanism in myocardial ischemic injury.
作者
刘志华
马晨光
LIU Zhihua1, MA Chenguang2(1.Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen 518055, China ; 2. Beijing Institute of YQ Medicine, Beijing 100022, China)
出处
《集成技术》
2018年第3期72-80,共9页
Journal of Integration Technology
基金
深圳市基础研究(JCYJ20150401145529007)
深圳市科技计划(CXZZ20151015163619907
JSGG20160229123927512
KQJSCX20170331161941176)
关键词
极低密度脂蛋白受体
缺血性心肌损伤
缺氧缺血
very low density lipoprotein （VLDL） receptor
myocardial ischemic injury
hypoxia-ischemia
