Coenzyme Q10: mitochondrial energy, oxidative protection and cardiovascular health
One of the most basic changes that occurs with ageing is a decline in the efficiency of the mitochondria, the powerhouses of our cells. This decline leads to less ATP production, more oxidative stress, and increased vulnerability of tissues with a high energy demand, such as the heart, the muscles, and the brain. Coenzyme Q10 (CoQ10) plays a central role in precisely these processes and therefore directly relates to several Hallmarks of Aging, including mitochondrial dysfunction, inflammaging, and disturbed intercellular communication.¹
CoQ10 is a fat-soluble molecule that occurs naturally in almost all cells of the body. In mitochondria, CoQ10 serves as an essential electron carrier within the electron transport chain, the system responsible for the production of ATP. Without enough CoQ10, this process runs inefficiently, causing energy production to fall and the formation of reactive oxygen species to increase. At the same time, CoQ10 functions as an endogenous antioxidant that can limit oxidative damage and counteract lipid peroxidation.¹
As we grow older, the body's own production of CoQ10 decreases. This effect is strengthened in people who use statins, since these medicines inhibit the same biosynthesis pathway as CoQ10, which can result in a lower CoQ10 status and an increased sensitivity to energy shortage and oxidative stress in energy-intensive tissues such as the heart muscle and skeletal muscles.
The health benefits of CoQ10 are fairly well supported in human studies, especially within the field of heart health. In the Q-SYMBIO study, a randomized, double-blind, multicentre trial, patients with chronic heart failure received CoQ10 for two years as an addition to standard care. Compared with placebo, the CoQ10 group showed a significant improvement in symptom scores, functional class, and a lower risk of cardiovascular death and major adverse cardiovascular events (MACE).²
In addition, meta-analyses show that CoQ10 supplementation can generally help lower systolic blood pressure, which is relevant for slowing cardiovascular ageing and reducing risk factors for heart and blood vessel diseases.³
Animal and preclinical studies further support these findings. CoQ10 supplementation in animal models improves mitochondrial function, supports oxidative phosphorylation, and reduces oxidative damage, which fits with the role of CoQ10 as a key factor in energy balance and antioxidant protection.
Taken together, this outlines a consistent biological picture: Coenzyme Q10 supports not just one part of health, but acts on basic mechanisms that determine how cells function as we grow older. By supporting mitochondrial energy production and protecting against oxidative stress, CoQ10 can contribute to maintaining cardiovascular function, physical energy, and cellular resilience.
CoQ10 is therefore an essential building block within a longevity strategy aimed at maintaining energy, heart health, and functional capacity in the long term—precisely the factors that determine how healthily we grow older.
- Metabolic Targets of Coenzyme Q10 in Mitochondria: https://pmc.ncbi.nlm.nih.gov/articles/PMC8066821/
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Q-SYMBIO RCT: randomized, double-blind multicentre study:
https://pubmed.ncbi.nlm.nih.gov/25282031/ -
Meta-analysis of CoQ10 and systolic blood pressure:
https://pubmed.ncbi.nlm.nih.gov/40495903/
