Genetic <i>Ace2</i> Deficiency Accentuates Vascular Inflammation and Atherosclerosis in the <i>ApoE</i> Knockout Mouse

Abstract

Genetic Ace2 deficiency is associated with upregulation of putative mediators of atherogenesis and enhances responsiveness to proinflammatory stimuli. In atherosclerosis-prone ApoE KO mice, these changes potentially contribute to increased plaque accumulation. These findings emphasize the potential utility of ACE2 repletion as a strategy to reduce atherosclerosis.