Coenzyme Q homeostasis in aging: Response to non-genetic interventions

• Published in: Free radical biology & medicine Vol. 164; pp. 285 - 302
• Main Author: López-Lluch, Guillermo
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 20-02-2021
• Subjects: Age-related diseases; Aging; Calorie restriction; Coenzyme Q; Mitochondria; Oxidative damage; Polyphenols; Reactive oxygen species; Mitochondria; Reactive oxygen species; Oxidative damage; Calorie restriction; Aging; Polyphenols; Coenzyme Q; Age-related diseases
• ISSN: 0891-5849; 1873-4596
• DOI: 10.1016/j.freeradbiomed.2021.01.024

Coenzyme Q (CoQ) is a key component for many essential metabolic and antioxidant activities in cells in mitochondria and cell membranes. Mitochondrial dysfunction is one of the hallmarks of aging and age-related diseases. Deprivation of CoQ during aging can be the cause or the consequence of this mitochondrial dysfunction. In any case, it seems clear that aging-associated CoQ deprivation accelerates mitochondrial dysfunction in these diseases. Non-genetic prolongevity interventions, including CoQ dietary supplementation, can increase CoQ levels in mitochondria and cell membranes improving mitochondrial activity and delaying cell and tissue deterioration by oxidative damage. In this review, we discuss the importance of CoQ deprivation in aging and age-related diseases and the effect of prolongevity interventions on CoQ levels and synthesis and CoQ-dependent antioxidant activities.
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•Aging-related mitochondrial dysfunction is associated with reduction of CoQ levels.•Prolongevity effectors modulate CoQ10 levels in an organ-specific effect.•Prolongevity effectors induce CoQ-dependent antioxidant activities.•CoQ synthesis, mitochondrial dynamics and turnover could share regulatory mechanisms no yet determined.•Maintenance of CoQ10 homeostasis may be essential for healthy aging.