According to the WHO, ischemic heart disease is the biggest killer of death worldwide, and atherosclerotic lesions in coronary arteries are one of the main causes of the disease. In the primary stages of atherosclerosis, a variety of risk factors which include hyperlipidemia, hypertension (Hurtubise et al., 2016), smoking (Fu et al., 2021), obesity, diabetes mellitus (Bhupathiraju and Hu, 2016; Rocha and Libby, 2009), and abnormal blood flow (Vancheri et al., 2020) can result in impaired endothelial cells and disrupted vessel wall integrity. The impaired endothelial barrier function causes lipid deposition and recruitment of monocytes into endothelium to differentiate into macrophages that uptake lipids and release inflammatory factors, further exacerbating endothelial injury. Smooth muscle cells from the intima also migrates to the endothelium, where it uptakes lipids together with macrophages and differentiates into “foam cells” (Ley et al., 2011). A large number of inflammatory cells enter the endothelium and release reactive oxygen species (ROS) to induce programmed death of different cells in the plaque (Förstermann et al., 2017). Both macrophage-derived and smooth muscle cell-derived foam cells within the plaque may undergo programmed cell death such as apoptosis, pyroptosis, and ferroptosis during the development of atherosclerosis, and these cells may accelerate plaque progression through the secretion of proinflammatory and chemotactic factors which further recruit leukocytes which inducing an amplifying effect of the inflammatory cascade (Bäck et al., 2019). Oxidative stress within atherosclerotic plaques also stimulates vascular smooth muscle cells to proliferate and secrete large amounts of extracellular matrix, which contributes to vascular sclerosis and lumen narrowing, thus affecting the blood supply to tissues and organs (Durham et al., 2018). Oxidative stress also induces the formation of atherosclerotic unstable plaques that are prone to rupture and lead to thrombosis, causing clinical acute cardiovascular events (Badimon and Vilahur, 2014). Therefore, clinical treatments for atherosclerosis are currently focused on controlling lipid levels and combating oxidative stress.

Coenzyme Q10 (CoQ10) is a lipid-soluble molecule widely found in cells. As a component of the mitochondrial respiratory chain, CoQ10 participates in cellular energy metabolism via the transportation of electrons (Milenkovic et al., 2017). CoQ10 is able to scavenge reactive oxygen species and is one of the important endogenous antioxidants, exerting anti-inflammatory effects outside the mitochondria. It also protects cells from damage by inhibiting oxidative stress and improving mitochondrial dysfunction (Quinzii et al., 2010). In addition to regulating intracellular redox homeostasis, CoQ10 also regulates lipid synthesis (Xu et al., 2017).

This review firstly summarized the physilogical function of CoQ10 in cells, such as acts as electron transporter, anti-oxidative stress, regulation of lipid metabolism and cellular autophagy and how these functions play roles in anti-atherosclerosis through some crucial phases in atherosclerosis including abnormal lipid metabolism, endothelial cell inflammation, foam cell formation, and plaque rupture. Subsequently, the research progress on the clinical application of CoQ10 in combination with drugs in recent years was discussed, especially its prophylactic and therapeutic significance. Lastly, as a healthcare product which need to be taken for a long time, the safety of CoQ10 were talked in the summary section of this review supported by experiments. However, Further studies are still needed to determine the therapeutic efficacy of CoQ10 on atherosclerosis alone, the different effects on people of different ages, and the specific mechanism of CoQ10 et al.

In this review, articles were identified through a PubMed search, as all journals were PubMed indexed. The studies (studies means the experiments in vitro/in vivo/clinical findings and other reviews) used in this study covers a period 33 years starting from 1990 2023.