Oxidative stress and inflammatory state jointly promote the occurrence of endothelial dysfunction (ED), which can cause the imbalance of oxidative and antioxidant balance reactions in cells, leading to a cascade reaction of signaling pathways and an increase in inflammatory markers such as NADPH oxidase, adhesion molecules, COX-2, tumor necrosis factor α, interleukin-6, CRP, 8-hydroxydeoxyguanosine, 3-nitrotyrosine, and monocyte chemoattractant proteins [32–34]. Here, FMO5 is linked to endothelial dysfunction.