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Objective— To test the hypothesis that chronic infusion of angiotensin-(1–7) [Ang-(1–7)] may dose-dependently inhibit atherosclerotic lesion formation by targeting vascular smooth muscle cells and a large dose of Ang-(1–7) may stabilize mature plaque by targeting macrophages. Approach and Results— In vivo, the effects of Ang-(1–7) on atherogenesis and plaque stability were observed in ApoE−/− mice fed a high-fat diet and chronic angiotensin II infusion. In vitro, the effects of Ang-(1–7) on vascular smooth muscle cells’ proliferation and migration, and macrophage inflammatory cytokines were examined. Ang-(1–7) dose-dependently attenuated early atherosclerotic lesions and inhibited vascular smooth muscle cells’ proliferation and migration via suppressing extracellular regulated protein kinase/P38 mitogen-activated protein kinase and janus kinase/signal transducers and activators of transcription activities and enhancing smooth muscle 22α and angiotensin II type 2 receptor expression. Ang-(1–7) treatment resulted in high contents of collagen and vascular smooth muscle cells, and low contents of macrophages and lipids in carotid mature plaques. Ang-(1–7) lowered the expression levels of proinflammatory cytokines and activities of matrix metalloproteinases in mature plaques.Conclusions— Ang-(1–7) treatment inhibits early atherosclerotic lesions and increases plaque stability in ApoE−/− mice, thus providing a novel and promising approach to the treatment of atherosclerosis.

Angiotensin-(1–7) Dose-Dependently Inhibits Atherosclerotic Lesion Formation and Enhances Plaque Stability by Targeting Vascular Cells