氨基肽酶 A:治疗高血压的新靶点

IF 2.8 3区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY
Pragya Sharma, Suman Sharma, Sarvesh Paliwal, Smita Jain
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引用次数: 0

摘要

肾素-血管紧张素系统(RAS)对于调节和了解高血压的病理生理学至关重要。然而,人们很少关注活性肽血管紧张素 II(AngII)的分解。鉴于缺乏氨基肽酶 A(APA)的动物表现出高血压,可以得出结论,APA 是通过分解 AngII 来调节血压的一种关键酶。研究还发现,自发性高血压大鼠(SHR)的血压升高是由于 RAS 被激活,同时肾脏血管紧张素转换酶(ACE)的活性降低所致。子痫前期开始时,APA 的活性会升高,随着子痫前期的进展(尤其是严重病例),APA 的活性会降低到正常妊娠时的水平以下。血清 APA 的活性在激素替代治疗(HRT)后也会升高,这可能是对 AngII 水平升高的一种反应。因此,研究 RAS 的激活、血液中 AngII 的水平以及高血压情况下 APA 的存在之间的联系至关重要。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Aminopeptidase A: A Novel Therapeutic Target for Hypertension Management

The renin-angiotensin system (RAS) is crucial for regulating and understanding the pathophysiology of hypertension. However, there has been little focus on the breakdown of the active peptide, angiotensin II (AngII). Given that animals lacking aminopeptidase A (APA) exhibit hypertension, it may be concluded that APA is a crucial enzyme in regulating blood pressure by breaking down AngII. It has been also seen that the elevated blood pressure in the spontaneously hypertensive rat (SHR) is caused by the activation of the RAS and a concurrent reduction in renal angiotensin-converting enzyme (ACE) activity. The activity of APA is elevated at the beginning of pre-eclampsia and decreases below the levels seen during a normal pregnancy as pre-eclampsia progresses (particularly, in severe cases). The activity of Serum APA is also heightened after hormone replacement treatment (HRT), perhaps as a response to increasing levels of AngII. Therefore, it is crucial to examine the connection between the activation of the RAS, the levels of AngII in the bloodstream, and the presence of APA in hypertension conditions.

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来源期刊
Cell Biochemistry and Function
Cell Biochemistry and Function 生物-生化与分子生物学
CiteScore
6.20
自引率
0.00%
发文量
93
审稿时长
6-12 weeks
期刊介绍: Cell Biochemistry and Function publishes original research articles and reviews on the mechanisms whereby molecular and biochemical processes control cellular activity with a particular emphasis on the integration of molecular and cell biology, biochemistry and physiology in the regulation of tissue function in health and disease. The primary remit of the journal is on mammalian biology both in vivo and in vitro but studies of cells in situ are especially encouraged. Observational and pathological studies will be considered providing they include a rational discussion of the possible molecular and biochemical mechanisms behind them and the immediate impact of these observations to our understanding of mammalian biology.
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