期刊文献+
任意字段
题名或关键词
题名
关键词
文摘
作者
第一作者
机构
刊名
分类号
参考文献
作者简介
基金资助
栏目信息

锌指蛋白转录因子KLFs家族与心血管疾病 被引量：4

下载PDF
导出
摘要 心血管疾病（cardiovasculardisease）是一系列与心脏血管相关的循环系统疾病。循环系统是指人体内运送血液的器官和组织，主要包括心脏和血管（动脉、静脉、微血管）。心血管疾病以血管病变为主要病理特征，其主要诱因包括炎症反应、内皮细胞损伤、脂代谢异常、血栓和动脉粥样硬化等。在诸多心血管疾病中，危害性最大患病人数最多的有心肌肥大、动脉粥样硬化、糖尿病、冠心病及肥胖等。
作者 邹小舟 杨晶 杨永玉 胡长平
机构地区 中南大学药学院药理学系 郑州大学附属第一医院药剂科
出处 《中南医学科学杂志》 CAS 2013年第4期325-331,共7页 Medical Science Journal of Central South China
基金 国家自然科学基金(81273512)
关键词 锌指蛋白转录因子KLFs家族 心血管疾病
分类号 R363 [医药卫生—病理学]
  • 相关文献

参考文献52

  • 1De Boer OJ,Vander Wal AC, Becker AE. Atherosclerosis, inflammation, and infection [ J ]. J Pathol,2000,190 ( 3 ) : 237 -243.
  • 2Atkins GB, Wang YM, Mahabeleshwar GH, et al. Hemizy- gous deficiency of Krtippel-like factor 2 augments experi- mental atherosclerosis [ J ]. Cir Res, 2008, 103 (7) : 690-693.
  • 3SenBanerjee S, Lin Z, Atkins GB, et al. KLF2 is a novel transcriptional regulator of endothelial proinflammatory ac- tivation [ J]. J Exp Med,2004,199(10) :1305-1315.
  • 4Dekker R J, van Soest S, Fontijn RD, et al. Prolonged fluid shear stress induces a distinct set of endothelial cell genes, most specifically lung Krtippel-like factor (KLF2) [ J ]. Blood, 2002,100 ( 5 ) : 1689-1698.
  • 5Kumar A, Lin Z, SenBanerjee S, et al. Tumor necrosis fac- tor alpha-mediated reduction of KLF2 is due to inhibition of MEF2 by NF-kappaB and histone deacetylases [ J ]. Mol Cell Biol, 2005,25 (14) :5893-5903.
  • 6Atkins GB, Jain MK. Role of Krtippel-like transcription factors in endothelial biology [ J]. Cire Res, 2007, 100 (12) : 1686-1695.
  • 7Parmar KM, Larman HB, Dai G, et al. Integration of flow- dependent endothelial phenotypes by Krtippel-like factor 2 [ J ]. J Clin Invest, 2006,116 ( 1 ) :49-58.
  • 8Dekker R J, Boon RA, Rondaij MG, et al. KLF2 provokes a gene expression pattern that establishes functional quies- cent differentiation of the endothelium [ J ]. Blood, 2006, 107( 11 ) :4354-4363.
  • 9Lin Z, Kumar A, SenBanerjee S, et al. Kriippel-like factor 2 (KLF2) regulates endothelial thrombotic function [ J ]. Circ Res, 2005,96 ( 5 ) : 48-57.
  • 10Bhattacharya R, Senbanerjee S, Lin Z, et al. Inhibition of vascular permeability factor/vascular endothelial growth factor-mediated angiogenesis by the Kriippel-like factor KLF2 [J]. J Biol Chem,2005,280(32):28848-28851.

同被引文献32

  • 1de CatesAN, FarrMR, WrightN, et al. Fixed-dose combination therapy for the prevention of cardiovascular disease[J]. Cochrane Database Syst Rev, 2014, 4:CD009868.
  • 2LiX, RenY, SorokinV, et al. Quantitative profiling of the rat heart myoblast secretome reveals differential responses to hypoxia and re-oxygenation stress[J]. J Proteomics, 2014, 98:138–149.
  • 3ShimokawaharaH, JougasakiM, SetoguchiM, et al. Relationship between vascular endothelial growth factor and left ventricular dimension in patients with acute myocardial infarction[J]. J Cardiol, 2014, 64(5):360–365.
  • 4FriehsI, MargossianRE, MoranAM, et al. Vascular endothelial growth factor delays onset of failure in pressure-overload hypertrophy through matrix metalloproteinase activation and angiogenesis[J]. Basic Res Cardiol, 2006, 101(3):204–213.
  • 5FischS, GrayS, HeymansS, et al. Kruppel-like factor 15 is a regulator of cardiomyocyte hypertrophy[J]. Proc Natl Acad Sci U S A, 2007, 104(17):7074–7079.
  • 6KaramanolisG, DelladetsimaI, KoulouliasV, et al. Increased expression of VEGF and CD31 in postradiation rectal tissue:implications for radiation proctitis[J]. Mediators Inflamm, 2013, 2013:515048.
  • 7SchramK, GangulyR, NoEK, et al. Regulation of MT1-MMP and MMP-2 by leptin in cardiac fibroblasts involves Rho/ROCK-dependent actin cytoskeletal reorganization and leads to enhanced cell migration[J]. Endocrinology, 2011, 152(5):2037–2047.
  • 8CorreiaC, GraysonWL, ParkM, et al. In vitro model of vascularized bone: synergizing vascular development and osteogenesis[J]. PLoS One, 2011, 6(12):e28352.
  • 9JiangY, WangH, CulpD, et al. Targeting Müller cell-derived VEGF164 to reduce intravitreal neovascularization in the rat model of retinopathy of prematurity[J]. Invest Ophthalmol Vis Sci, 2014, 55(2):824–831.
  • 10LaroumanieF, Douin-EchinardV, PozzoJ, et al. CD4+ T cells promote the transition from hypertrophy to heart failure during chronic pressure overload[J]. Circulation, 2014, 129(21):2111–2124.

引证文献4

二级引证文献5

中南医学科学杂志
2013年 第4期

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部