Coenzyme Q10 Supplementation in Aging and Disease

Abstract

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 retard the onset of these diseases. Here, we review the current knowledge of CoQ10 biosynthesis and primary CoQ10 deficiency syndrome, and have collected published results from clinical trials based on CoQ10 supplementation. 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. There is a need for further studies and clinical trials involving a greater number of participants undergoing longer treatments in order to assess the benefits of CoQ10 treatment in metabolic syndrome and diabetes, neurodegenerative disorders, kidney diseases, and human fertility.

Coenzyme Q 10 alleviates tacrolimus‐induced mitochondrial dysfunction in kidney

“…The main role of CoQ 10 in cells is participation in the electron transport chain of the inner mitochondrial membrane (20). CoQ 10 contributes to the control of cell redox status via modulation of ROS generation.…”

Aging‐induced Akt activation involves in aging‐related pathologies and Aβ‐induced toxicity

“…Molecular signals found to be changed during aging are sometimes also altered in neurodegenerative diseases (Colacurcio & Nixon, ; Jagust, ; Winick‐Ng & Rylett, ). There are many similarities between an aged animal and an animal with a neurodegenerative disease; for instance, (a) accumulated oxidative stress is observed in both animals (Hernández‐Camacho, Bernier, López‐Lluch & Navas, ; Hussain et al., ; Prolla & Mattson, ), (b) the requirement of nutrition is increased (Harding, Gonder, Robinson, Crean & Singhrao, ; Prolla & Mattson, ), (c) learning and memory performance decline, and (d) multicellular signals are altered in the brain. However, whether there is one common cellular pathway that links and regulates both aging‐related pathologies and neurodegenerative diseases remains unclear.…”

Ubiquinol Ameliorates Endothelial Dysfunction in Subjects with Mild-to-Moderate Dyslipidemia: A Randomized Clinical Trial

“…Although the role of CoQ10 has extensively been explored in healthy subjects and in different pathological conditions, its effects on EF have mainly been described in patients with CVD and related chronic states such as type 2 diabetes and CAD [46,47]. In a study involving CoQ10 supplementation in healthy non-smokers with hypercholesterolemia, Raitakari et al found baseline FMD values that were comparable to those observed in our population, lending support to the notion that hypercholesterolemia alone is sufficient to induce ED in the absence of other risk factors.…”