Activation of Nrf2 inhibits atherosclerosis in ApoE mice through suppressing endothelial cell inflammation and lipid peroxidation

Abstract

Upon HCD feeding in ApoE^-/- mice, endothelial inflammation is an earliest event, followed by the appearance of LPO. EC-specific activation of Nrf2 inhibits atherosclerosis while EC-specific knockdown of Nrf2 results in the opposite effect. Pharmacological activators of endothelial Nrf2 may represent a novel therapeutic strategy for the treatment of atherosclerosis.