动脉粥样硬化与脑梗死危险因素

被引:15
作者
王位
黎红华
机构
[1] 广州军区武汉总医院
关键词
动脉粥样硬化; 危险因素; 内皮功能; 氧化应激; 炎症;
D O I
暂无
中图分类号
R543.5 [动脉疾病];
学科分类号
摘要
<正>动脉粥样硬化(AS)是动脉血管壁上一种多因素共同参与的复杂的慢性病变,是心脑血管疾病的重要病理基础,其病因和发病机制尚未完全清楚。但近期研究表明,一些脑梗死危险因素和AS密切相关,及时消除或减少这些危险因素,可减缓AS的进展。现将AS主要发病机制及其与脑梗死危险因素的关系综述如下。1 AS发生的主要机制近年来信号转导和基因调控方面的研究结果揭示炎症和氧化应激是AS发生的两个关键机制,是AS从脂肪条纹形成到斑块破裂和血栓形成这一发展过程的主要环节。而内皮功能障碍是AS的始动环节。1.1炎症与AS在AS斑块形成的起始阶段,血中白细胞
引用
收藏
页码:109 / 111
页数:3
相关论文
共 14 条
  • [1] 代谢综合征内皮功能紊乱与大血管病变的研究进展
    卢细娇
    潘海林
    [J]. 医学综述, 2010, (11) : 1705 - 1708
  • [2] 剪切力对脑微血管内皮细胞形态学的影响
    胡金麟
    宋欣
    李向红
    [J]. 中国生物医学工程学报, 2000, (03) : 247 - 250
  • [3] C-reactive protein down-regulates endothelial nitric oxide synthase expression and promotes apoptosis in endothelial progenitor cells through receptor for advanced glycation end-products
    Chen, Jianfei
    Jin, Jun
    Song, Minbao
    Dong, Hongmei
    Zhao, Can
    Huang, Lan
    [J]. GENE, 2012, 496 (02) : 128 - 135
  • [4] Free Fatty Acid Causes Leukocyte Activation and Resultant Endothelial Dysfunction Through Enhanced Angiotensin II Production in Mononuclear and Polymorphonuclear Cells
    Azekoshi, Yoko
    Yasu, Takanori
    Watanabe, Saiko
    Tagawa, Tatsuya
    Abe, Satomi
    Yamakawa, Ken
    Uehara, Yoshinari
    Momomura, Shinichi
    Urata, Hidenori
    Ueda, Shinichiro
    [J]. HYPERTENSION, 2010, 56 (01) : 136 - U218
  • [5] Effect of the Metabolic Syndrome and Hyperuricemia on Outcome in Patients With Coronary Artery Disease (from the Bezafibrate Infarction Prevention Study)
    Brodov, Yafim
    Behar, Shlomo
    Boyko, Valentina
    Chouraqui, Pierre
    [J]. AMERICAN JOURNAL OF CARDIOLOGY, 2010, 106 (12) : 1717 - 1720
  • [6] Impaired Endothelial Progenitor Cell Activity is Associated with Reduced Arterial Elasticity in Patients with Essential Hypertension
    Yang, Zhen
    Chen, Long
    Su, Chen
    Xia, Wen-Hao
    Wang, Yan
    Wang, Jie-Mei
    Chen, Fei
    Zhang, Yuan-Yuan
    Wu, Fang
    Xu, Shi-Yue
    Zhang, Xiao-Lin
    Tao, Jun
    [J]. CLINICAL AND EXPERIMENTAL HYPERTENSION, 2010, 32 (07) : 444 - 452
  • [7] Mechanisms of fibrinogen‐induced microvascular dysfunction during cardiovascular disease[J] . D.Lominadze,W. L.Dean,S. C.Tyagi,A. M.Roberts.Acta Physiologica . 2009 (1)
  • [8] Human C-reactive protein induces endothelial dysfunction and uncoupling of eNOS in vivo
    Hein, Travis W.
    Singh, Uma
    Vasquez-Vivar, Jeannette
    Devaraj, Sridevi
    Kuo, Lih
    Jialal, Ishwarlal
    [J]. ATHEROSCLEROSIS, 2009, 206 (01) : 61 - 68
  • [9] Tetrahydrobiopterin, superoxide, and vascular dysfunction[J] . Jeannette Vásquez-Vivar.Free Radical Biology and Medicine . 2009 (8)
  • [10] Acute inhibition of guanosine triphosphate cyclohydrolase 1 uncouples endothelial nitric oxide synthase and elevates blood pressure
    Wang, Shuangxi
    Xu, Jian
    Song, Ping
    Wu, Yong
    Zhang, Junhua
    Choi, Hyoung Chul
    Zou, Ming-Hui
    [J]. HYPERTENSION, 2008, 52 (03) : 484 - 490