血管紧张素（1-7）/Mas——肺部疾病治疗的新靶点
网络出版日期: 2015-09-30
基金资助
国家自然科学基金（81272145）
Angiotensin-(1-7)/Mas: novel therapeutic targets for treatment of pulmonary diseases
Online published: 2015-09-30
Supported by
National Natural Science Foundation of China， 81272145
肺组织是血管紧张素转化酶(ACE)表达和血管紧张素Ⅱ(AngⅡ)生成的主要场所。已有研究表明肾素—血管紧张素系统(RAS)参与了急性呼吸窘迫综合征、肺动脉高压、肺纤维化、哮喘及肺癌的发病过程。RAS内存在ACE/AngⅡ/血管紧张素Ⅱ 1型受体(AT1R)和血管紧张素转化酶2(ACE2)/血管紧张素(1-7)[Ang-(1-7)]/Mas两大轴系。AngⅡ通过其特异性受体AT1R参与了多种肺部疾病的发生与进展，而Ang-(1-7)通过作用于其特异性受体Mas发挥对抗AngⅡ的作用。文章对Ang-(1-7)/Mas在几种常见肺部疾病中的保护性作用及其可能的分子机制进行综述。
关键词： 血管紧张素（1-7）; Mas; 血管紧张素Ⅱ; 肺疾病
刘玉静 , 李颖川 . 血管紧张素（1-7）/Mas——肺部疾病治疗的新靶点[J]. 上海交通大学学报（医学版）, 2015 , 35(9) : 1379 . DOI: 10.3969/j.issn.1674-8115.2015.09.027
Lung is a major site for the expression of angiotensin-converting enzyme (ACE) and generation of angiotensin Ⅱ (AngⅡ). Studies have showed that the renin-angiotensin system (RAS) involves in the pathogenesis of acute respiratory distress syndrome, pulmonary fibrosis, pulmonary hypertension, asthma, and lung cancer. There are two axes in the RAS, i.e. the ACE/AngⅡ/angiotensin Ⅱ type 1 receptor (AT1R) axis and the ACE2/angiotensin-(1-7) [Ang-(1-7)]/Mas axis. AngⅡ involves in the incidence and development of many pulmonary diseases through its specific receptor AT1R, while Ang-(1-7) counteracts the effect of AngⅡ via specific receptor Mas. This paper reviews the protective effect and possible molecular mechanisms of Ang-(1-7)/Mas during the course of several common pulmonary diseases.
Key words： angiotensin-(1-7); Mas; angiotensin Ⅱ; pulmonary disease
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