Key result
Activation of the renin-angiotensin system induces monocyte/macrophage pro-inflammatory polarization, leading to endothelial dysfunction, fibrosis, oxidative stress, and end-organ damage in hypertension.
Pharmacological targeting of renin-angiotensin system components in monocyte/macrophages may present an innovative strategy for the treatment of hypertension and related end-organ damage.
Highlights immune pathways as adjunct targets in hypertension; leaves open whether modulation improves outcomes beyond RAS blockade.
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.
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Barhoumi et al. (2023) conducted a review in Hypertension and end-organ damage. Renin-angiotensin system activation was evaluated. Activation of the renin-angiotensin system induces monocyte/macrophage pro-inflammatory polarization, leading to endothelial dysfunction, fibrosis, oxidative stress, and end-organ damage in hypertension.
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