Atherosclerosis and Toll-Like Receptor4 (TLR4), Lectin-Like Oxidized Low-Density Lipoprotein-1 (LOX-1), and Proprotein Convertase Subtilisin/Kexin Type9 (PCSK9)

<div>LOX-1, PCSK9, and TLR4 functions in EC. Overall, activated NF-<i>κ</i>B upregulates the expression of inflammatory cytokines, such as IL-6, IL-1, and TNF-<i>α</i>. As shown, HMGB1 activity causes a decrease in the activity of eNOS. NADPH oxidase is a key mediator of the LOX-1-PCSK9 axis. Upon its activation, there will be an increase in ROS production, which is an inducer for PCSK9 production and further impairment of the function of endothelial cells. ROS, reactive oxygen species; HMGB1, high mobility group box 1 protein; TLR4, Toll-like receptor 4; eNOS, endothelial nitric oxide synthase.</div>

Mediators of Inflammation

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Figure 3: Atherosclerosis and Toll-Like Receptor4 (TLR4), Lectin-Like Oxidized Low-Density Lipoprotein-1 (LOX-1), and Proprotein Convertase Subtilisin/Kexin Type9 (PCSK9) 

Figure 3 | Atherosclerosis and Toll-Like Receptor4 (TLR4), Lectin-Like Oxidized Low-Density Lipoprotein-1 (LOX-1), and Proprotein Convertase Subtilisin/Kexin Type9 (PCSK9) 