Atherosclerosis (AS) is one of the main causes of cardiovascular diseases, and its complex pathophysiological mechanism involves the interaction of multiple factors. Laminar shear stress (LSS) plays a key role in the regulation of AS processes, but its specific mechanism is still unclear. In this study, we analyzed the proteome data of static culture and LSS-treated human aortic endothelial cells (HAECs), to explore the role and potential mechanism of LSS in AS.