Coenzyme Q was firstly discovered by Frederick Crane and his team, in 1957. The most common form of humane Coenzyme Q is believed to be Coenzyme Q10, which acts as a cofactor in oxidative phosphorylation of adenosine triphosphate (ATP). In the oxidative phosphorylation process, might be oxidized (Ubiquinone) or reduced (Ubiquinol). Cellular bioenergetics depends on the appropriate activation of these cofactors that has led to clinical usage of them in problems involving tissues with high metabolic needs, such as heart muscle. The agent also has anti-inflammatory impacts as it suppresses the expression of tumor necrosis factor alpha (TNF-a) gene. In addition, CoQ10 is an antioxidant, and reduces reactive oxygen species (ROS). The agent has similarities with vitamins; however, it shouldn’t be categorized as vitamin, because the body produces. The effect of on the cardiovascular system was understudy since the discovery of the agent. Previous studies showed that deficiency could be present in variety of cardiovascular disorders such as mitral valve disease, aortic valve disease, cardiomyopathies, congenital alular defects, ischemic heart disease, and myocardial infarction. Concentration was lower in the myocardium of patients with heart failure. Also, levels are lower in smoker subjects and patients who suffer from hyperlipidemia.

While, it has been mentioned the concentration could not use as a sole indicator of cardiovascular diseases. Previous reports also showed that the administration of could be helpful in both prevention and treatment of cardiovascular diseases. The published evidence showed that supplementation could have several therapeutic effects for diseases of different organs because of its anti-inflammatory and anti-oxidative properties. In the present study we aimed to review the beneficial impacts of on cardiovascular diseases Atherosclerosis is defined as the collection of lipid and cholesterol sediments within the sub-endothelial space of arteries leading to chronic inflammation. Atherosclerotic cardiovascular disease is among the main causes of death, worldwide. The immune system and inflammatory response play a decisive role in initiation and progression of atherosclerotic changes, that the condition could be classified into inflammatory diseases. Besides, the mitochondrial dysfunction could result in the progression of disease, as it increases ROS activities, and oxidative stress damages. Prescription could be a promising alternative treatment for atherosclerosis, as it could regulate inflammation, mitochondrial energy, gene expression, oxidative state of cell membranes.

CoQ10 supplementation in Apo-lipoprotein E deficient mice fed with a high-fat diet resulted in improvement of atherosclerotic lesions. Other studies on animal models showed same results, since they had a preventing role on induction of atherosclerosis in mice. A controlled, double-blind, randomized trial showed that with a dosage of 120 mg daily combined with aged garlic extract could improve the inflammatory markers of coronary atherosclerosis, and slow down the disease progression. Myocardial infarction (MI) is a medical condition that can lead to considerable rates of morbidity and mortality. MI could be among the first manifestations of CAD, or it might happen, recurrently, in cases with the diagnosed disease. It is believed that the prescription of could be beneficial in patient with MI, and the underlying mechanisms are assumed to be the improvement of mitochondrial dysfunction and mitigation of DNA damage by anti-oxidative effect of the agent.

Best Regards,
Nancy Ella
Associate Managing Editor
Drug Designing: Open Access