局部血管紧张素 II/血管紧张素 1 型受体在子宫内膜异位症中的作用:新治疗方法的潜在目标。

Shirin Moazen, Mohammad-Hassan Arjmand
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引用次数: 0

摘要

子宫内膜异位症是一种慢性炎症性疾病,其特征是在子宫外位置存在功能性子宫内膜样组织,与慢性盆腔疼痛和不孕症有关。包括炎症、活性氧(ROS)生成、纤维化反应和血管生成在内的多种分子机制参与了子宫内膜异位症的发病机制;然而,这种疾病的确切病因仍是一个有待讨论的问题。最近的研究表明,局部肾素-血管紧张素系统(RAS)在妇科等不同组织中均有表达,其表达的改变与子宫内膜异位症等多种病症有关。血管紧张素 II(Ang II)作为 RAS 的主要肽,通过血管紧张素 1 型受体(AT1R)上调核因子卡巴 B(NF-κB)、丝裂原活化蛋白激酶(MAPK)和转化生长因子 beta(TGF-β)等信号转导通路,从而促进炎症、氧化应激和纤维增生。血管紧张素受体阻滞剂(ARB)可控制因 AT1R 活性过高而升高的高血压。最近,人们认识到血管紧张素受体阻滞剂因其抗炎和抗纤维化作用而具有组织保护作用。在这篇综述中,我们重点探讨了局部Ang II/AT1R轴活性在子宫内膜异位症发病机制中的作用,并论证了使用ARB药物作为改善子宫内膜异位症的潜在治疗策略的合理性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The Role of Local Angiotensin II/Angiotensin Type 1 Receptor in Endometriosis: A Potential Target for New Treatment Approaches

Endometriosis is a chronic inflammatory disorder described by the presence of functional endometrial-like tissues at extra-uterine locations that are related to chronic pelvic pain and infertility. Multiple molecular mechanisms, including inflammation, reactive oxygen species (ROS) generation, fibrotic reactions, and angiogenesis, are involved in the pathogenesis of endometriosis; however, the exact cause of this disorder still remains a matter of discussion. Recently, it has been shown that the local renin-angiotensin system (RAS) has been expressed in different tissues, like the gynecological tract, and alterations in its expression are associated with multiple pathological conditions like endometriosis. Angiotensin II (Ang II), as a main peptide of the RAS through angiotensin type 1 receptor (AT1R), upregulates signal transduction pathways such as nuclear factor kappa B (NF-κB), mitogen activation protein kinase (MAPK), and transforming growth factor beta (TGF-β) to promote inflammation, oxidative stress, and fibrogenesis. Angiotensin receptor blockers (ARBs) control high blood pressure, which is increased by excessive AT1R activity. Recently, it has been recognized that ARBs have tissue protective effects because of their anti-inflammatory and antifibrotic effects. In this review, we focused on the role of local Ang II/AT1R axis activity in endometriosis pathogenesis and justified the use of ARB agents as a potential therapeutic strategy to improve endometriosis.

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