肾素血管紧张素系统与微炎症
作者:
作者单位:

作者简介:

通讯作者:

中图分类号:

基金项目:


Renin-angiotensin system and micro-inflammation
Author:
Affiliation:

Fund Project:

  • 摘要
  • |
  • 图/表
  • |
  • 访问统计
  • |
  • 参考文献
  • |
  • 相似文献
  • |
  • 引证文献
  • |
  • 资源附件
  • |
  • 文章评论
    摘要:

    高血压、糖尿病、脂质代谢紊乱和肥胖常常簇集出现而形成代谢综合征, 严重影响公众的健康水平。近年来, 代谢性疾病的微炎症背景备受学者关注, 微炎症状态与代谢性疾病的发生发展密切关联。肾素-血管紧张素系统(RAS), 除了血流动力学调节作用外, 在微炎症反应中也发挥重要的作用。阻断RAS, 对代谢性疾病具有一定的保护作用。目前已证实, RAS主要通过血管紧张素转换酶-血管紧张素Ⅱ-AT1受体(ACE-AngⅡ-AT1R)轴和ACE2-Ang(1-7)-Mas轴发挥作用, 这两条途径具有相反的生物学活性, 后者对前者有拮抗作用。血管紧张素Ⅱ(AngⅡ)由血管紧张素Ⅱ受体介导通过多种机制发挥致炎作用, 而Ang(1-7)可以拮抗AngⅡ, 抑制炎症反应。本文就RAS参与微炎症反应的相关机制做一综述。

    Abstract:

    The cluster of hypertension, diabetes mellitus, dyslipidemia and body obesity, collectively referred to as the metabolic syndrome, is a common cause of atherosclerotic and cardiovascular diseases, and also one of the most serious threats to public health. Metabolic syndrome is closely related to micro-inflammation, which receives great attention in recent years. Besides the hemodynamic regulatory role, renin-angiotensin system (RAS) also plays an important role in micro-inflammation. Blockade of RAS could protect against the development of metabolic syndrome. It has been confirmed that RAS exerts its effects mainly through angiotensin converting enzyme(ACE)-angiotensinⅡ(AngⅡ)-angiotensin 1 receptor(AT1R) axis and ACE2-Ang(1-7)-Mas axis, and the two approaches have opposite biological activities. Angiotensin(Ang)Ⅱ could initiate inflammation through a variety of mechanisms by its receptors, but the Ang1-7, as the antagonists to AngⅡ, restrains the inflammation. In this paper, we reviewed the mechanism through which RAS is involved in micro-inflammation.

    参考文献
    相似文献
    引证文献
引用本文

赵 珏, 窦京涛.肾素血管紧张素系统与微炎症[J].中华老年多器官疾病杂志,2012,11(2):146~149

复制
分享
文章指标
  • 点击次数:
  • 下载次数:
  • HTML阅读次数:
  • 引用次数:
历史
  • 收稿日期:
  • 最后修改日期:
  • 录用日期:
  • 在线发布日期:
  • 出版日期: