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

Tlili Barhoumi; Stephen Todryk

doi:10.3389/fphys.2023.1199934

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

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

Authors

Tlili Barhoumi^{1

2}, Stephen Todryk³

Affiliations

¹ 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.
² King Saud Bin Abdulaziz University for Health Sciences, Riyadh, Kingdom of Saudi Arabia.
³ Department of Applied Sciences, Northumbria University, Newcastle Upon Tyne, United Kingdom.

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.

Keywords: hypertension; innate immunity; macrophages; monocytes; renin-angiotensin system.

Publication types

Review

Grants and funding

This review article was supported by grant from King Abdullah International Research Center no. RC18/171/R. The authors extend their appreciation to Research/funding Platforms at King Abdullah International Medical Research Center (KAIMRC) for supporting and funding project (RC18/171/R).