Coenzyme Q (CoQ) is an essential component of the mitochondrial electron transport chain and an antioxidant in plasma membranes and lipoproteins. It is endogenously produced in all cells by a highly regulated pathway that involves a mitochondrial multiprotein complex. Defects in either the structural and/or regulatory components of CoQ complex or in non-CoQ biosynthetic mitochondrial proteins can result in a decrease in CoQ concentration and/or an increase in oxidative stress. Besides CoQ10 deficiency syndrome and aging, there are chronic diseases in which lower levels of CoQ10 are detected in tissues and organs providing the hypothesis that CoQ10 supplementation could alleviate aging symptoms and/or slows the onset of these diseases.

There is evidence that supplementation positively affects mitochondrial deficiency syndrome and the symptoms of aging based mainly on improvements in bioenergetics. Cardiovascular disease and inflammation are alleviated by the antioxidant effect of CoQ10.

Myocardial deficiency of CoQ 10 has been demonstrated in endomyocardial biopsy samples from patients with cardiomyopathy, and deficiency of CoQ 10 correlated with the severity of disease, suggesting that therapy with CoQ 10 can result in improving the quality of life of cardiac patients by enhancing myocardial contractility. Numerous studies have investigated the benefit of CoQ 10 supplementation for improving cardiovascular function via enhanced energy production, improved contractility of cardiac muscles, and its potent antioxidant activity, particularly the prevention of low-density lipoproteins oxidation.

Advances in molecular medicine have provided novel insights into the pathophysiology of heart disease. Coenzyme Q10 (CoQ10) exerts action at the cellular level and rectifies some of the basic deficiencies leading to aggravation of these diseases. These include correction of the energy depletion and oxidant stress which are inherent in these conditions.