Other studies have reported that Gal3 can exacerbate endothelial dysfunction through a signaling pathway mediated by oxidized low-density lipoprotein receptor-1 (LOX-1) and may also be mediated by the LOX-1/ROS/p38/NF-κB signaling pathway, which induces inflammation and exacerbates endothelial dysfunction [93]. This evidence concerns the gene LGALS3 and endothelial dysfunction.