The angiotensin-(1-7)/mas receptor axis in macrophage-mediated vascular inflammation: A narrative review

Introduction Angiotensin-(1-7) (Ang-(1-7)) is a central bioactive component of the renin-angiotensin system (RAS) that counter-regulates angiotensin II signaling via the Mas receptor, thereby maintaining cardiovascular and immune homeostasis. Beyond its vasoprotective effects, the Ang-(1-7)/Mas axis has been increasingly recognized as an important immunomodulatory pathway influencing macrophage biology and vascular inflammation. Methods This narrative review was based on a comprehensive evaluation of experimental, translational, and clinical evidence addressing the role of the Ang-(1-7)/Mas axis in macrophage-mediated vascular inflammation. The literature was critically appraised with emphasis on macrophage phenotype modulation, inflammatory signaling, vascular remodeling, and the therapeutic potential of targeting this protective RAS pathway. Results Ang-(1-7)/Mas signaling suppresses pro-inflammatory macrophage activation, promotes reparative phenotypes, enhances efferocytic and phagocytic functions, and facilitates resolution of inflammation. At the vascular level, this pathway reduces macrophage infiltration, leukocyte recruitment, and endothelial activation, contributing to plaque stabilization and attenuation of adverse remodeling. Emerging evidence highlights receptor cross-talk within the RAS network and context-dependent effects shaped by lesion stage and systemic milieu. Conclusions The Ang-(1-7)/Mas axis represents a promising translational target linking vascular immunobiology with novel therapeutic strategies for macrophage-driven cardiovascular disease. Further experimental and clinical studies are warranted to define its potential across diverse vascular inflammatory settings.