索引超出了数组界限。 文章摘要
|本期目录/Table of Contents|

[1]申广辉,曹丽娟,陈福祥.人巨细胞病毒感染促动脉粥样硬化的机制[J].国际心血管病杂志,2017,05:285-288.
点击复制

人巨细胞病毒感染促动脉粥样硬化的机制(PDF)

《国际心血管病杂志》[ISSN:1006-6977/CN:61-1281/TN]

期数:
2017年05期
页码:
285-288
栏目:
综述
出版日期:
2017-10-20

文章信息/Info

Title:
-
作者:
申广辉; 曹丽娟; 陈福祥
200011 上海交通大学医学院附属第九人民医院检验科(申广辉,陈福祥),心内科(曹丽娟)
Author(s):
-
关键词:
人巨细胞病毒;  动脉粥样硬化;  炎症反应;  脂质代谢异常
Keywords:
-
分类号:
-
DOI:
10.3969/j.issn.1673-6583.2017.05.009
文献标识码:
-
摘要:
人巨细胞病毒(human cytomegalovirus, HCMV)是以潜伏感染为主的双链DNA病毒。研究发现,HCMV感染可能是 动脉粥样硬化的致病因素。HCMV感染可通过模式识别受体激活单核-巨噬细胞和淋巴细胞,触发炎症反应; 也可促进被感 染细胞摄入氧化低密度脂蛋白诱发脂质累积,从而导致动脉粥样硬化的发生发展。该文介绍HCMV诱发动脉粥样硬化炎症 反应和脂质代谢异常的机制。
Abstract:
-

参考文献/References

[1] Pasterkamp G, den Ruijter HM, Libby P. Temporal shifts in clinical presentation and underlying mechanisms of atherosclerotic disease[J]. Nat Rev Cardiol, 2017, 14(1):21-29.
[2] Maiolino G, Rossitto G, Caielli P, et al. The role of oxidized low-density lipoproteins in atherosclerosis: the myths and the facts[J]. Mediators Inflamm, 2013, 2013:714653.
[3] Jia YJ, Liu J, Han FF, et al. Cytomegalovirus infection and atherosclerosis risk: a meta-analysis [J]. J Med Virol, 2017 May 17. [Epub ahead of print]
[4] Nikitskaya E, Lebedeva A, Ivanova O, et al. Cytomegalovirus-productive infection is associated with acute coronary syndrome[J]. J Am Heart Assoc, 2016, 5(8):e003759.
[5] Chatzidimitriou D, Kirmizis D, Gavriilaki E, et al. Atherosclerosis and infection: is the jury still not in?[J]. Future Microbiol, 2012, 7(10):1217-1230.
[6] Huygens A, Dauby N, Vermijlen D, et al. Immunity to cytomegalovirus in early life[J]. Front Immunol, 2014, 5:552.
[7] Ji YN, An L, Zhan P, et al. Cytomegalovirus infection and coronary heart disease risk: a meta- analysis[J]. Mol Biol Rep, 2012, 39(6):6537-6546.
[8] Horváth R, Cerný J, Benedík J, et al. The possible role of human cytomegalovirus(HCMV)in the origin of atherosclerosis[J]. J Clin Virol, 2000, 16(1):17-24.
[9] Yaiw KC, Ovchinnikova O, Taher C, et al. High prevalence of human cytomegalovirus in carotid atherosclerotic plaques obtained from Russian patients undergoing carotid endarterectomy[J]. Herpesviridae, 2013, 4(1):3.
[10] Blum A, Peleg A, Weinberg M. Anti-cytomegalovirus(CMV)IgG antibody titer in patients with risk factors to atherosclerosis[J]. Clin Exp Med, 2003, 3(3):157-160.
[11] Durose JB, Li J, Chien S, et al. Infection of vascular endothelial cells with human cytomegalovirus under fluid shear stress reveals preferential entry and spread of virus in flow conditions simulating atheroprone regions of the artery[J]. J Virol, 2012, 86(24):13745-13755.
[12] Seo JY, Cresswell P. Viperin regulates cellular lipid metabolism during human cytomegalovirus infection[J]. PLoS Pathog, 2013, 9(8):e1003497.
[13] Zhou YF, Guetta E, Yu ZX, et al. Human cytomegalovirus increases modified low density lipoprotein uptake and scavenger receptor mRNA expression in vascular smooth muscle cells[J]. J Clin Invest, 1996, 98(9):2129-2138.
[14] Tanaka K, Zou JP, Takeda K, et al. Effects of human cytomegalovirus immediate-early proteins on p53-mediated apoptosis in coronary artery smooth muscle cells[J]. Circulation, 1999, 99(13):1656-1659.
[15] Qiu H, Strååt K, Rahbar A, et al. Human CMV infection induces 5-lipoxygenase expression and leukotriene B4 production in vascular smooth muscle cells[J]. J Exp Med, 2008, 205(1):19-24.
[16] Zischke J, Mamareli P, Pokoyski C, et al. The human cytomegalovirus glycoprotein pUL11 acts via CD45 to induce T cell IL-10 secretion[J]. PLoS Pathog, 2017, 13(6):e1006454.
[17] Yu Y, Maguire TG, Alwine JC. Human cytomegalovirus activates glucose transporter 4 expression to increase glucose uptake during infection[J]. J Virol, 2011, 85(4):1573-1580.
[18] Ma Y, He B. Recognition of herpes simplex viruses: toll-like receptors and beyond[J]. J Mol Biol, 2014, 426(6):1133-1147.
[19] Smith PD, Shimamura M, Musgrove LC, et al. Cytomegalovirus enhances macrophage TLR expression and MyD88-mediated signal transduction to potentiate inducible inflammatory responses[J]. J Immunol, 2014, 193(11):5604-5612.
[20] Rott D, Zhu J, Zhou YF, et al. IL-6 is produced by splenocytes derived from CMV-infected mice in response to CMV antigens, and induces MCP-1 production by endothelial cells: a new mechanistic paradigm for infection-induced atherogenesis[J]. Atherosclerosis, 2003, 170(2):223-228.
[21] Smith MS, Bivins-Smith ER, Tilley AM, et al. Roles of phosphatidylinositol 3-kinase and NF-kappaB in human cytomegalovirus-mediated monocyte diapedesis and adhesion: strategy for viral persistence[J]. J Virol, 2007, 81(14):7683-7694.
[22] Fu YZ, Su S, Gao YQ, et al. Human cytomegalovirus tegument protein UL82 inhibits STING-mediated signaling to evade antiviral immunity[J]. Cell Host Microbe, 2017, 21(2):231-243.

备注/Memo

备注/Memo:
通信作者:陈福祥,Email:fuxiang_chen@hotmail.com
更新日期/Last Update: 2017-10-20