Endothelial injury mechanism and transendothelial transport of oxidized lipoprotein. The expression of LOX-1 is enhanced with an increase in TNF-\alpha, IL-1, and ox-LDL levels. LOX-1 paired with ox-LDL directly generates superoxide anion ROS, and LPC, an important component of ox-LDL, and it can also boost the NOX activity and promote the conversion of NO to ROS. The increased ROS stimulates the expression of associated target genes, such as MCP-1, ICAM-1, and VCAM-1, through the NF-\kappaB pathway and ultimately enhances monocyte recruitment and pro-transformation function of endothelial cells. In contrast, decreased NO has weakened vasodilatory and anticoagulant effects, which is manifested as weakened anti-atherosclerotic function of endothelial cells. Through the P13K/AKT/mTORC1 pathway, ox-LDL inhibits the key regulator of autophagy ULK1, attenuates the autophagy of endothelial cells, and promotes the development of local lesions. Oxidized lipoproteins can cross the endothelium monolayer by convection and/or diffusion between neighboring cells (paracellular leak) or transcytosis via individual cells. Transcytosis may be receptor-mediated or may occur by fluid-phase pinocytosis; it is also possible that transcellular channels may contribute to this process. By this mechanism, oxidized lipoproteins can permeate the basal membrane and participate in the subsequent development of plaques.