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连接黏附分子-A与心血管疾病的关系——从基础到临床 被引量:2

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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。
出处 《国际心血管病杂志》 2016年第3期161-163,共3页 International Journal of Cardiovascular Disease
基金 上海申康适宜技术推广项目(SHDC12012210) 宝山区科委项目(12-E-63)
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参考文献17

  • 1Cavusoglu E,Kornecki E, Sobocka MB, et al. Association of plasma levels of F11 receptor/junctional adhesion molecule-A(F11R/JAM A) with human atheroselerosis [J] . J Am Coil Cardiol, 2007,50 (18) : 1768-1776.
  • 2Tokat B, Kurt O, Bugra Z, et al. Investigation of the monoeyte diapedesis-related LEA-1 and JAMA gene variants in Turkish coronary heart disease patients [J] . Meta gene, 2014,2:1-10.
  • 3Babinska A,Clement CC,Swiatkowska M,et al. Development of new antiatherosclerotic and antithrombotic drugs utilizing Fll 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. 被引量:18
  • 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. 被引量:15
  • 6Schmitt 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.
  • 7Kang 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.
  • 8Koenen 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.
  • 9Huang 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.
  • 10Naik 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.

二级参考文献31

  • 1Koenen RR, Weber C. Chemokines: established and noveltargets in atherosclerosis [J]. EMBO Mol Med, 2011,3(12); 713-725.
  • 2Kadi A, Meher AK* Sharma PR,et al. Identification of anovel macrophage phenotype that develops in response toatherogenic phospholipids via Nr.2 [ J Circ Res, 2010,107(6): 737-746.
  • 3Stoger JL, Gijbels MJ,van der Velden S,et al. Distributionof macrophage polarization markers in human atherosclerosis[J]. Atherosclerosis, 2012, 225(2) : 461-468.
  • 4Gui T, Shimokado A, Sun Y, et al. Diverse roles of macrophagesin atherosclerosis: from inflammatory biology to biomarkerdiscovery[J]. Mediators Inflamm, 2012,2012;693083.
  • 5Woollard KJ,Geissmann F. Monocytes in atherosclerosis :subsets and functions [J]. Nat Rev Cardiol, 2010,7(2):77-86.
  • 6Makinen PI, Lappalainen JP,Heinonen SE, et al. Silencingof either SR-A or CD36 reduces atherosclerosis inhyperlipidaemic mice and reveals reciprocal upregulation ofthese receptors[J]. Cardiovasc Res, 2010,88(3) : 530-538.
  • 7Little PJ,Chait A, Bobik A. Cellular and cytokine-basedinflammatory processes as novel therapeutic targets for theprevention and treatment of atherosclerosis [J]. PharmacolTher, 2011,131(3) : 255-268.
  • 8Businaro R, Tagliani A* Buttari B,et al. Cellular and molecularplayers in the atherosclerotic plaque progression^Jl. Ann NY Acad Sci, 2012,1262 : 134-141.
  • 9Go GW, Mani A. Low-density lipoprotein receptor (LDLR)family orchestrates cholesterol homeostasis [J]. Yale J BiolMed, 2012,85(1) : 19-28.
  • 10Moore KJ, Tabas I. Macrophages in the pathogenesis ofatherosclerosis[J]. Cell, 2011,145(3) : 341-355.

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