LOX-1 has been reported to be responsible for the uptake and degradation of ox-LDL, and its expression has been shown in vitro to be upregulated by a number of atherosclerosis-related stimuli including shear stress, inflammatory cytokines [such as IL-1β and tumor necrosis factor alpha (TNFα)], and conditions such as hypertension (Mitra et al., 2011; Pirillo et al., 2013). This evidence concerns the gene OLR1 and atherosclerosis.