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单核细胞/巨噬细胞在肾素-血管紧张素系统诱导的高血压和终末器官损伤中的作用。

Role of monocytes/macrophages in renin-angiotensin system-induced hypertension and end organ damage.

作者信息

Barhoumi Tlili, Todryk Stephen

机构信息

Medical Research Core Facility and Platforms (MRCFP), King Abdullah International Medical Research Center, King Saud Bin Abdulaziz University for Health Sciences (KSAU-HS), Riyadh, Saudi Arabia.

King Saud Bin Abdulaziz University for Health Sciences, Riyadh, Kingdom of Saudi Arabia.

出版信息

Front Physiol. 2023 Oct 3;14:1199934. doi: 10.3389/fphys.2023.1199934. eCollection 2023.

DOI:10.3389/fphys.2023.1199934
PMID:37854465
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10579565/
Abstract

The renin-angiotensin system (RAS) is a central modulator of cardiovascular physiology. Pathophysiology of hypertension is commonly accompanied by hyper-activation of RAS. Angiotensin II receptor blockers (ARBs) and Angiotensin-converting enzyme (ACE) inhibitors are the gold standard treatment for hypertension. Recently, several studies highlighted the crucial role of immune system in hypertension. Angiotensin-II-induced hypertension is associated with low grade inflammation characterized by innate and adaptive immune system dysfunction. Throughout the progression of hypertension, monocyte/macrophage cells appear to have a crucial role in vascular inflammation and interaction with the arterial wall. Since myelomonocytic cells potentially play a key role in angiotensin-II-induced hypertension and organ damage, pharmacological targeting of RAS components in monocyte/macrophages may possibly present an innovative strategy for treatment of hypertension and related pathology.

摘要

肾素-血管紧张素系统(RAS)是心血管生理学的核心调节因子。高血压的病理生理学通常伴随着RAS的过度激活。血管紧张素II受体阻滞剂(ARBs)和血管紧张素转换酶(ACE)抑制剂是高血压的金标准治疗药物。最近,多项研究强调了免疫系统在高血压中的关键作用。血管紧张素II诱导的高血压与以先天性和适应性免疫系统功能障碍为特征的低度炎症相关。在高血压的整个进展过程中,单核细胞/巨噬细胞似乎在血管炎症以及与动脉壁的相互作用中起关键作用。由于骨髓单核细胞可能在血管紧张素II诱导的高血压和器官损伤中起关键作用,因此对单核细胞/巨噬细胞中RAS成分进行药物靶向治疗可能为高血压及相关病理状况的治疗提供一种创新策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/36f6/10579565/8df5e054a72d/FPHYS_fphys-2023-1199934_wc_abs.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/36f6/10579565/8df5e054a72d/FPHYS_fphys-2023-1199934_wc_abs.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/36f6/10579565/8df5e054a72d/FPHYS_fphys-2023-1199934_wc_abs.jpg

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