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

[1]陈一竹,张俊峰.连接黏附分子-A与心血管疾病的关系——从基础到临床[J].国际心血管病杂志,2016,03:161-163.
点击复制

连接黏附分子-A与心血管疾病的关系——从基础到临床(PDF)

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

期数:
2016年03期
页码:
161-163
栏目:
综述
出版日期:
2016-05-20

文章信息/Info

Title:
-
作者:
陈一竹; 张俊峰
200020 上海交通大学医学院附属第三人民医院
Author(s):
-
关键词:
连接黏附分子-A; 动脉粥样硬化; 血小板; 内皮细胞; 上皮细胞
Keywords:
-
分类号:
-
DOI:
10.3969/j.issn.1673-6583.2016.03.009
文献标识码:
-
摘要:
连接黏附分子-A(JAM-A)属于免疫球蛋白超家族,是一种跨膜蛋白,在动脉粥样硬化等多种心血管疾病的病理生理过程中发挥重要作用。该文主要介绍JAM-A与心血管疾病关系的基础与临床研究。
Abstract:
-

参考文献/References

[1] Cavusoglu E,Kornecki E,Sobocka MB,et al. Association of plasma levels of F11 receptor/junctional adhesion molecule-A(F11R/JAM-A)with human atherosclerosis [J]. J Am Coll Cardiol,2007,50(18):1768-1776.
[2] Tokat B,Kurt O,Bugra Z,et al. Investigation of the monocyte diapedesis-related LFA-1 and JAM-A gene variants in Turkish coronary heart disease patients [J]. Meta gene,2014,2:1-10.
[3] Babinska A,Clement CC,Swiatkowska M,et al. Development of new antiatherosclerotic and antithrombotic drugs utilizing F11 receptor(F11R/JAM-A)peptides [J]. Biopolymers,2014,101(4):322-334.
[4] 石 健,侯静波. 基质金属蛋白酶与动脉粥样硬化关系研究新进展 [J]. 国际心血管病杂志,2013,40(1):25-27.
[5] 何流漾,赵建中,戚春建. 免疫细胞在动脉粥样硬化中的作用 [J]. 国际心血管病杂志, 2013,40(3):139-141.
[6] Schmitt MM,Fraemohs L,Hackeng TM,et al. Atherogenic mononuclear cell recruitment is facilitated by oxidized lipoprotein-induced endothelial junctional adhesion molecule-A redistribution [J]. Atherosclerosis,2014,234(2):254-264.
[7] Kang LI,Wang Y,Suckow AT,et al. Deletion of JAM-A causes morphological defects in the corneal epithelium [J]. Int J Biochem Cell Biol,2007,39(3):576-585.
[8] Koenen RR,Pruessmeyer J,Soehnlein O,et al. Regulated release and functional modulation of junctional adhesion molecule A by disintegrin metalloproteinases [J]. Blood,2009,113(19):4799-4809.
[9] Huang H,Cruz F,Bazzoni G. Junctional adhesion molecule-A regulates cell migration and resistance to shear stress [J]. J Cell Physiol,2006,209(1):122-130.
[10] Naik MU,Caplan JL,Naik UP. Junctional adhesion molecule-A suppresses platelet integrin alphaIIbbeta3 signaling by recruiting Csk to the integrin-c-Src complex [J]. Blood,2014,123(9):1393-1402.
[11] Karshovska E,Zhao Z,Blanchet X,et al. Hyperreactivity of junctional adhesion molecule A-deficient platelets accelerates atherosclerosis in hyperlipidemic mice [J]. Circ Res,2015,116(4):587-599.
[12] Schmitt MM,Megens RT,Zernecke A,et al. Endothelial junctional adhesion molecule-a guides monocytes into flow-dependent predilection sites of atherosclerosis [J]. Circulation,2014,129(1):66-76.
[13] Woodfin A,Reichel CA,Khandoga A,et al. JAM-A mediates neutrophil transmigration in a stimulus-specific manner in vivo: evidence for sequential roles for JAM-A and PECAM-1 in neutrophil transmigration [J]. Blood,2007,110(6):1848-1856.
[14] Zernecke A,Liehn EA,Fraemohs L,et al. Importance of junctional adhesion molecule-A for neointimal lesion formation and infiltration in atherosclerosis-prone mice [J]. Arterioscler Thromb Vasc Biol,2006,26(2):e10-e13.
[15] Xu H,Oliveira-Sales EB,McBride F,et al. Upregulation of junctional adhesion molecule-A is a putative prognostic marker of hypertension [J]. Cardiovasc Res,2012,96(3):552-560.
[16] Giannotta M,Benedetti S,Tedesco FS,et al. Targeting endothelial junctional adhesion molecule-A/EPAC/Rap-1 axis as a novel strategy to increase stem cell engraftment in dystrophic muscles [J]. EMBO Mol Med,2014,6(2):239-258.
[17] Corada M,Chimenti S,Cera MR,et al. Junctional adhesion molecule-A-deficient polymorphonuclear cells show reduced diapedesis in peritonitis and heart ischemia-reperfusion injury [J]. Proc Nal Acad Sci USA,2005,102(30):10634-10639.

备注/Memo

备注/Memo:
基金项目:上海申康适宜技术推广项目(SHDC12012210); 宝山区科委项目(12-E-63) 作者单位:200020 上海交通大学医学院附属第三人民医院 心内科 通信作者:张俊峰,Email:jfzhang_dr@163.com
更新日期/Last Update: 2016-05-20