HDL signaling and protection against coronary artery atherosclerosis in mice

作     者：Bernardo L Trigatti Mark Fuller 

作者机构：Department of Biochemistry and Biomedical SciencesMcMaster University and Thrombosis and Atherosclerosis Research InstituteMcMaster University and Hamilton Health Sciences 

出 版 物：《The Journal of Biomedical Research》 (生物医学研究杂志（英文版）)

年 卷 期：2016年第30卷第2期

页      面：94-100页

核心收录：

学科分类：1002[医学-临床医学] 100201[医学-内科学(含：心血管病、血液病、呼吸系病、消化系病、内分泌与代谢病、肾病、风湿病、传染病)] 10[医学] 

基　　金：supported by funds from the Canadian Institutes of Health Research (MOP74765) the Heart and Stroke Foundation of Canada(G-13-0002833 and G-15-0009016) 

主　　题：coronary artery disease high density lipoprotein myocardial infarction scavenger receptor class B type 1 

摘      要：Atherosclerosis is a leading underlying factor in cardiovascular disease and stroke,important causes of morbidity and mortality across the *** epidemiological studies demonstrate that high levels of high density lipoprotein（HDL） are associated with reduced risk of atherosclerosis and preclinical,animal model studies demonstrate that this association is *** the molecular mechanisms underlying the protective effects of HDL will allow more strategic approaches to development of HDL based *** evidence suggests that an important aspect of the ability of HDL to protect against atherosclerosis is its ability to trigger signaling responses in a variety of target cells including endothelial cells and macrophages in the vessel *** signaling responses require the HDL receptor,scavenger receptor class B type 1（SR-B1）,an adaptor protein（PDZK1） that binds to the cytosolic C terminus of SR-B1,Akt1 activation and（at least in endothelial cells） activation of endothelial NO synthase（eNOS）.Mouse models of atherosclerosis,exemplified by apolipoprotein E or low density lipoprotein receptor gene inactivated mice（apoE or LDLR KO） develop atherosclerosis in their aortas but appear generally resistant to coronary artery *** the other hand,inactivation of each of the components of HDL signaling（above）in either apoE or LDLR KO mice renders them susceptible to extensive coronary artery atherosclerosis suggesting that HDL signaling may play an important role in protection against coronary artery disease.