Apelin is the endogenous ligand of APJ receptor. Both monocytes (MCs) and human umbilical vein endothelial cells (HUVECs) express apelin and APJ, which play important roles in the physiological processes of atherosclerosis. Our previous research indicated that apelin‐13 promoted MCs‐HUVECs adhesion. Here, we further explore the mechanism responsible for MCs‐HUVECs adhesion induced by apelin‐13. Apelin‐13 promoted reactive oxygen species (ROS) generation and NOX4 expression in HUVECs. Apelin‐13 inducedautophagy, increased proteins beclin1 and LC3‐II/I expression and induced autophagy flux in HUVECs, which was blocked by NAC, catalase and DPI. Autophagy flux induced by apelin‐13 was inhibited by NAC and catalase but not hydroxychloroquine (HCQ). NAC, catalase, and DPI prevented apelin‐13 induced ICAM‐1 expression in HUVECs. Rapamycin enhanced MCs–HUVECs adhesion that was reversed by NAC, catalase, and DPI. Down‐regulation of beclin1 and LC3 by siRNA blocked MCs‐HUVECs adhesion. Apelin‐13 induced atherosclerotic plaque and increased NOX4, LC3‐II/I expression in ApoE−/−(HFD) mouse model. Our results demonstrated that apelin‐13 induced MCs–HUVECs adhesion via a ROS‐autophagy pathway. Apelin‐13 increased ROS expression and induced autophagy in HUVECs. ROS‐autophagy pathway mediated monocytes‐HUVECs adhesion induced by apelin‐13.