Tier 3 — preclinical

Understanding coenzyme Q

Ying Wang, Noah Lilienfeldt, Siegfried Hekimi
Physiological Reviews 2024 104(4):1533-1610

Bibliography

PubMed
PMID 38722242
PubMed Central
PMC11495197
DOI
10.1152/physrev.00040.2023
Funding
Supported by the Canadian Institutes of Health Research, grant FDN-159916 to Siegfried Hekimi.
Competing interests
The authors declared no conflicts of interest, financial or otherwise.

Study snapshot

DesignComprehensive peer-reviewed physiological review
ModelBasic, translational and human coenzyme Q biology across mitochondrial, membrane, redox and deficiency literature
SampleNot applicable — review article
InterventionNo intervention; synthesis of CoQ physiology, biosynthesis, deficiency and supplementation literature
DurationNot applicable
EndpointsCoQ chemical structure and membrane localization; Mitochondrial electron transport; Redox biology and antioxidant/pro-oxidant roles; CoQ biosynthesis; Primary CoQ deficiency; Secondary CoQ deficiency; Limitations of oral CoQ supplementation

What the study showed, in plain terms

This 2024 Physiological Reviews article is a broad modern synthesis of coenzyme Q biology. CoQ is an extremely hydrophobic membrane molecule built from a benzoquinone head group and a long isoprenoid side chain. In humans, CoQ10 is synthesized endogenously and is best known for carrying electrons within the mitochondrial respiratory chain, but it also participates in multiple redox-dependent cellular processes.

The review emphasizes that CoQ is not simply an antioxidant supplement. Depending on its redox state and cellular context, it participates in electron transfer, antioxidant defense, reactive-oxygen-species biology and several enzyme systems. It is synthesized in cells and distributed across biological membranes.

The authors distinguish rare primary CoQ deficiency caused by mutations in biosynthetic genes from more common secondary reductions associated with other mitochondrial disorders and disease states. They also stress that oral supplementation does not automatically correct tissue deficiency because CoQ is highly hydrophobic and difficult to deliver to the relevant intracellular compartments.

Key findings

CoQ is a membrane-resident redox molecule whose canonical role is electron transport in the mitochondrial electron transport chain, supporting oxidative phosphorylation and ATP production.

CoQ is synthesized endogenously in metazoan cells and is present in most or potentially all biological membranes; its ubiquinone/ubiquinol redox cycling contributes to cellular redox balance.

Primary CoQ deficiency is a rare genetic disorder caused by defects in CoQ biosynthetic genes. Secondary CoQ deficiency can accompany a broader range of mitochondrial and pathological states.

The review cautions that raising circulating CoQ after oral supplementation is not equivalent to correcting tissue or organellar deficiency, because absorption, transport and intracellular delivery are major biological constraints.

What this study can and cannot tell us

This is a narrative physiological review rather than a systematic review or randomized intervention trial, so it is strongest for biological framing and mechanism rather than effect-size estimates for supplementation.

The review covers a very broad literature spanning model systems, genetics and human disease; findings from basic biology should not be converted directly into claims that oral CoQ10 supplementation improves health outcomes in generally healthy people.

The authors themselves emphasize that health benefits from oral CoQ consumption are not established across indications and that treatment of tissue deficiency remains challenging.

Citation network

Articles citing this research paper

8 articles

Biohack Blueprint analyses that reference this study in their evidence base.

Editorial review

Reviewed by the Biohack Blueprint research team

Last verified

Dr. Khaled Mahmoud, MBBChCritical Care Medicine, Longevity Science & Editorial Direction Dr. Amr Yasser, PhDCardiometabolic, Musculoskeletal, Gut & Bioavailability Dr. Abdulla Mostafa, PhDCellular Senescence, Neurological, Mitochondrial & Brain-Ageing Biology