TLR4 and atherosclerosis: Regarding the microbial assessments performed on Escherichia coli (E. coli) lipopolysaccharide (LPS), LPS could promote the LOX-1 mRNA expression through the TLR4/MyD88/ROS-activated p38MAPK/NF-κB pathway in endothelial cells [53], and based on our finding, this pathway might be a new possible regulatory mechanism for bilirubin through inhibiting the LOX-1 expression and atherosclerosis development.