Metabolism and function of coenzyme Q
Open accessAbstract
Coenzyme Q (CoQ) is present in all cells and membranes and in addition to be a member of the mitochondrial respiratory chain it has also several other functions of great importance for the cellular metabolism. This review summarizes the findings available to day concerning CoQ distribution, biosynthesis, regulatory modifications and its participation in cellular metabolism. There are a number of indications that this lipid is not always functioning by its direct presence at the site of action but also using e.g. receptor expression modifications, signal transduction mechanisms and action through its metabolites. The biosynthesis of CoQ is studied in great detail in bacteria and yeast but only to a limited extent in animal tissues and therefore the informations available is restricted. However, it is known that the CoQ is compartmentalized in the cell with multiple sites of biosynthesis, breakdown and regulation which is the basis of functional specialization. Some regulatory mechanisms concerning amount and biosynthesis are established and nuclear transcription factors are partly identified in this process. Using appropriate ligands of nuclear receptors the biosynthetic rate can be increased in experimental system which raises the possibility of drug-induced upregulation of the lipid in deficiency. During aging and pathophysiological conditions the tissue concentration of CoQ is modified which influences cellular functions. In this case the extent of disturbances is dependent on the localization and the modified distribution of the lipid at cellular and membrane levels.
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HMG-CoA blockade is more potent at inhibiting cholesterol biosynthesis than CoQ biosynthesis because of differing Km values for trans-prenyltransferase and squalene synthetase at the farnesyl-PP branch point.
“HMG-CoA blockade is more potent at inhibiting cholesterol biosynthesis than CoQ biosynthesis because of differing Km values for trans-prenyltransferase (leads to CoQ) and squalene synthetase (leads to cholesterol) at the farnesyl-PP branch point (315).”
From Mitochondrial Dysfunction in Diabetes: From Molecular Mechanisms to Functional Significance and Therapeutic Opportunities (2010) · cites this paper as [315]
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- Authors
- Turunen, M., Olsson, J., & Dallner, G.
- Affiliations
- Karolinska University Hospital (SE)
- Karolinska Institutet (SE)
- Stockholm University (SE)
- Corresponding author
- Dallner, Gustav
- Venue
- Biochimica et Biophysica Acta (BBA) - Biomembranes
- Publisher
- Elsevier BV
- Published
- 2004-01
- Volume
- 1660
- Issue
- 1-2
- Pages
- 171-199
- ISSN
- 0005-2736 (ISSN-L)
- OpenAlex
- W1971714188
- Cited by
- 1,026
- References
- 323
- Citations by year
- 2026: 20 · 2025: 36 · 2024: 34 · 2023: 47 · 2022: 63 · 2021: 61 · 2020: 71 · 2019: 49 · 2018: 46 · 2017: 47 · 2016: 49 · 2015: 72 · 2014: 55 · 2013: 44 · 2012: 43
- FWCI
- 8.73
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Biochimica et Biophysica Acta (BBA) - Biomembranes (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Coenzyme Q10 studies and effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Toxicology › Bioactive Compounds and Antitumor Agents
- Keywords
- coenzyme Q10, mitochondrial respiratory chain, coenzyme Q biosynthesis, cellular metabolism, nuclear transcription factors, nuclear receptors, signal transduction, aging, membrane localization
- MeSH terms
- Aging, Animals, Biological Transport, Diet, Escherichia coli, Half-Life, Humans, Mevalonic Acid, Oxidation-Reduction, Terpenes, Tissue Distribution, Ubiquinone, Models, Animal
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