Why the study?
While classical RAAS is established in blood pressure control, mounting evidence indicates immune cells possess an intrinsic RAAS influencing inflammatory processes and hypertension pathogenesis.
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Design
Review
Myeloid RAAS may drive hypertension inflammation; leaves open whether targeting it alters clinical outcomes.
This review explores the intersection of the renin-angiotensin-aldosterone system (RAAS) and myeloid cell biology, with particular focus on how their interaction contributes to hypertension pathogenesis and related inflammatory comorbidities. While the classical RAAS is well-established in systemic blood pressure control and fluid balance, evidence is mounting that immune cells possess an intrinsic RAAS that influences inflammatory processes. We highlight recent findings that myeloid cells not only respond to circulating RAAS factors but also express RAAS components, creating local autocrine/paracrine loops. We also examine emerging links between myeloid RAAS signaling and other conditions such as cardiometabolic disorders, autoimmune diseases, infections, and fibrosis, which suggest broad implications beyond blood pressure regulation.
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Albritton et al. (2026) studied this question.
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