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首页> 外文期刊>Therapeutic advances in cardiovascular disease. >Cardiac ACE2/angiotensin 1–7/Mas receptor axis is activated in thyroid hormone-induced cardiac hypertrophy
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Cardiac ACE2/angiotensin 1–7/Mas receptor axis is activated in thyroid hormone-induced cardiac hypertrophy

机译：甲状腺激素引起的心脏肥大中激活心脏ACE2 /血管紧张素1-7 / Mas受体轴

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Thyroid hormone (TH) promotes marked effects on the cardiovascular system, including the development of cardiac hypertrophy. Some studies have demonstrated that the renin–angiotensin system (RAS) is a key mediator of the cardiac growth in response to elevated TH levels. Although some of the main RAS components are changed in cardiac tissue on hyperthyroid state, the potential modulation of the counter regulatory components of the RAS, such as angiotensin-converting enzyme type 2 (ACE2), angiotensin 1–7 (Ang 1–7) levels and Mas receptor induced by hyperthyroidism is unknown. The aim of this study was to investigate the effect of hyperthyroidism on cardiac Ang 1–7, ACE2 and Mas receptor levels. Hyperthyroidism was induced in Wistar rats by daily intraperitoneal injections of T4 for 14 days. Although plasma Ang 1–7 levels were unchanged by hyperthyroidism, cardiac Ang 1–7 levels were increased in TH-induced cardiac hypertrophy. ACE2 enzymatic activity was significantly increased in hearts from hyperthyroid animals, which may be contributing to the higher Ang 1–7 levels observed in the T4 group. Furthermore, elevated cardiac levels of Ang 1–7 levels were accompanied by increased Mas receptor protein levels. The counter-regulatory components of the RAS are activated in hyperthyroidism and may be contributing to modulate the cardiac hypertrophy in response to TH.
机译：甲状腺激素（TH）对心血管系统有明显的促进作用，包括心脏肥大的发展。一些研究表明，肾素-血管紧张素系统（RAS）是TH水平升高时心脏生长的关键介质。尽管甲状腺功能亢进状态的心脏组织中一些主要的RAS成分发生了变化，但是RAS的反调节成分的潜在调节作用，例如2型血管紧张素转换酶（ACE2），1-7血管紧张素（Ang 1-7）甲亢引起的血红蛋白水平和Mas受体尚不清楚。这项研究的目的是研究甲状腺功能亢进症对心脏Ang 1-7，ACE2和Mas受体水平的影响。每天腹膜内注射T4持续14天，在Wistar大鼠中诱发甲亢。尽管甲状腺功能亢进使血浆Ang 1–7水平不变，但TH诱导的心脏肥大中心脏Ang 1–7水平升高。甲状腺功能亢进动物心脏中的ACE2酶活性显着增加，这可能是导致T4组中Ang 1–7水平升高的原因。此外，心脏Ang 1–7水平的升高伴随着Mas受体蛋白水平的升高。 RAS的反调节成分在甲状腺功能亢进症中被激活，并可能响应TH参与调节心脏肥大。

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