阻断肾素-血管紧张素系统的抗炎作用:未来展望

Karmand Salih Hamaamin, N. Mahmood
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引用次数: 0

摘要

肾素-血管紧张素系统(RAS)被认为负责控制血压和电解质。已经确定血管紧张素II除了控制血压和钾水平外,还负责控制炎症。血管紧张素转换酶2 (ACE2)、血管紧张素(1-7)、血管紧张素(1-9)和其他RAS成分已被确定,并具有抗血管紧张素II的作用。血管紧张素受体阻滞剂(ARBs)和血管紧张素转换酶抑制剂(ACEIs)都被用作抗高血压药物和保护心脏和肾脏,并抵消Ang II在炎症启动中的作用。这篇综述提供了关键的细节,有助于解释ACEI和ARBs如何减轻炎症。通过谷歌Scholar、PubMed和ResearchGate等可靠的网站,对最新的出版物进行了审查。搜索词包括“RAS在炎症中的作用”、“ACEI的影响”和“ARBs对ppar - γ的影响”。数据来自对照临床试验、体外研究和动物研究;预印本、文章综述和荟萃分析研究被排除在外。acei和arb都通过多种机制减轻炎症,这解释了它们的心脏保护和肾保护作用。它们通过相似或不同的机制调节炎症途径来减轻炎症。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Anti-inflammatory Role of Blocking the Renin-angiotensin System: Future Prospective
The renin-angiotensin system (RAS) was thought to be in charge of managing blood pressure and electrolytes. It has been established that angiotensin II is also responsible for controlling inflammation in addition to blood pressure and potassium levels. Angiotensin converting enzyme 2 (ACE2), angiotensins (1–7), angiotensins (1–9), and other additional RAS components have been identified, and have anti-angiotensin II effects. Both angiotensin receptor blockers (ARBs) and angiotensin converting enzyme inhibitors (ACEIs) are utilized as anti-hypertensive medications and protecting the heart and kidneys, and counteract the part played by Ang II in the initiation of inflammation. This review provides crucial details that help explain how ACEI and ARBs reduce inflammation. Using reliable websites like Google Scholar, PubMed, and ResearchGate, the most recent publications were reviewed. Search terms have included "RAS role of Ang II in inflammation," "influence of ACEI," and "effect of ARBs on PPAR-gamma." The data were gathered from controlled clinical trials, in vitro studies, and animal-based studies; preprints, article reviews, and meta-analysis studies were excluded. Both ACEIs and ARBs reduce inflammation via a variety of mechanisms, which explains their cardioprotective and nephroprotective effects. They reduce inflammation by modulating an inflammatory pathway through either similar or dissimilar mechanisms.
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