血管紧张素(1-7)/Mas——肺部疾病治疗的新靶点

Angiotensin-(1-7)/Mas:novel therapeutic targets for treatment of pulmonary diseases

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Ⅱ1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。

Lung is a major site for the expression of angiotensin-converting enzyme（ACE） and generation of angiotensin Ⅱ（Ang Ⅱ）.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/Ang Ⅱ/angiotensin Ⅱ type 1 receptor（AT1R） axis and the ACE2/angiotensin-（1-7）[Ang-（1-7）]/Mas axis.Ang Ⅱ involves in the incidence and development of many pulmonary diseases through its specific receptor AT1 R,while Ang-（1-7） counteracts the effect of Ang Ⅱvia 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.