Coenzyme Q10 in atherosclerosis

Atherosclerotic disease is a chronic disease that predominantly affects the elderly and is the most common cause of cardiovascular death worldwide. Atherosclerosis is closely related to processes such as abnormal lipid transport and metabolism, impaired endothelial function, inflammation, and oxidative stress. Coenzyme Q10 (CoQ10) is a key component of complex Ⅰ in the electron transport chain and an important endogenous antioxidant that may play a role in decelerating the progression of atherosclerosis. Here, the different forms of CoQ10 presence in the electron transport chain are reviewed, as well as its physiological role in regulating processes such as oxidative stress, inflammatory response, lipid metabolism and cellular autophagy. It was also found that CoQ10 plays beneficial effects in atherosclerosis by mitigating lipid transportation, endothelial inflammation, metabolic abnormalities, and thrombotic processes from the perspectives of molecular mechanisms, animal experiments, and clinical evidence. Besides, the combined use of CoQ10 with other drugs has better synergistic therapeutic effects. It seems reasonable to suggest that CoQ10 could be used in the treatment of atherosclerotic cardiovascular diseases while more basic and clinical studies are needed. CoQ10 plays an alleviating role in atherosclerosis.(Ⅰ)Lipid deposition in the vascular intima can stimulate the endothelium to produce inflammatory factors that attract monocyte aggregates. (Ⅱ)Next, Macrophages phagocytose lipids to form foam cells and release chemokines, which in turn promote differentiation of monocytes into macrophages. (Ⅲ)Besides, platelet adhesion and fibrin deposition can form thrombi on plaques. These factors cause atherosclerosis to worsen, but CoQ10 could slow down the process. (A)Coq10 could reduce circulating levels of oxidized LDL and TGs, increase HDL levels, (B)inhibit oxidative stress and inflammatory responses, (C)and slow down monocyte aggregation. (D)CoQ10 also reduces foam cell formation and decreases plaque size by promoting reverse cholesterol transport through ABCG1 and ABCA1. (E)In addition, it inhibits conformational activation of platelet αIIbβ3 integrin receptors.(Abbreviations: CoQ10: coenzyme Q10, LDL: low density lipoprotein, HDL: High density lipoprotein, TGs: triglycerides, RCT: Reverse Cholesterol Transport, ROS: Reactive Oxygen species, AMPK: AMP-activated protein kinase, TNF-α: Tumor Necrosis Factor α, VCAM-1: Vascular cell adhesion molecule-1, I