Several studies confirmed that in vivo deletion of LOX-1 in LDLR−/− mice fed with a high-fat diet for 18 weeks resulted in enhanced collagen deposition and attenuated atherosclerosis, while in vitro silencing of LOX-1 in macrophages reduced mtDNA damage, ROS accumulation, and NLRP3 activation [26–28]. This evidence concerns the gene OLR1 and atherosclerosis.