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Cited by 92Coenzyme Q10 studies and effectsLipoproteins and Cardiovascular HealthCancer, Lipids, and Metabolism

The Effect of HMG-CoA Reductase Inhibitors on Coenzyme Q10: Possible Biochemical/Clinical Implications

Hargreaves, Iain P, Duncan, Andrew J, Heales, Simon J R, Land, John M·2005·Drug Safety
DOI 10.2165/00002018-200528080-00002
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Abstract

The HMG-CoA reductase inhibitors, also known as statins, have an enviable safety profile; however, myotoxicity and to a lesser extent hepatotoxicity have been noted in some patients following treatment. Statins target several tissues, depending upon their lipophilicity, where they competitively inhibit HMG-CoA reductase, the rate-limiting enzyme for mevalonic acid synthesis and subsequently cholesterol biosynthesis. HMG-CoA reductase is also the first committed rate-limiting step for the synthesis of a range of other compounds including steroid hormones and ubidecarenone (ubiquinone), otherwise known as coenzyme Q(10) (CoQ(10)). Recent interest has focused on the possible role CoQ(10) deficiency may have in the pathophysiology of the rare adverse effects of statin treatment. Currently, there is insufficient evidence from human studies to link statin therapy unequivocally to pathologically significantly decreased tissue CoQ(10) levels. Although statin treatment has been reported to lower plasma/serum CoQ(10) status, few human studies have assessed tissue CoQ(10) status. The plasma/serum CoQ(10) level is influenced by a number of physiological factors and, therefore, has limited value as a means of assessing intracellular CoQ(10) status. In those limited studies that have assessed the effect of statin treatment upon tissue CoQ(10) levels, none have shown evidence of a fall in CoQ(10) levels. This may reflect the doses of statins used, since many appear to have been used at doses below those recommended for their maximum therapeutic effects. Moreover, the poor bioavailability in those peripheral tissues tested may not reflect the effects the agents are having in liver and muscle, the tissues commonly affected in those patients who do not tolerate statins. This article reviews the biochemistry of CoQ(10), its role in cellular metabolism and the available evidence linking possible CoQ(10) deficiency to statin therapy.

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  • Statins reduce cholesterol formation via the mevalonate pathway, and this pathway may also affect mitochondrial coenzyme Q10 formation.

    “Statins act via the mevalonate pathway to reduce the formation of cholesterol, but impingement of this pathway may also affect the formation of the mitochondrial cofactor, coenzyme Q 10 (Q 10 ) (11).”

    From Simvastatin Effects on Skeletal Muscle (2013) · cites this paper as [11]

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Authors
Hargreaves, I. P., Duncan, A. J., Heales, S. J. R., & Land, J. M.
Affiliations
  • National Hospital for Neurology and Neurosurgery (GB)
  • UCL Queen Square Institute of Neurology (GB)
Corresponding author
Hargreaves, Iain P
ORCID
Venue
Drug Safety
Publisher
Springer Science and Business Media LLC
Published
2005
Volume
28
Issue
8
Pages
659-676
ISSN
0114-5916 (ISSN-L)
DOI
10.2165/00002018-200528080-00002
OpenAlex
W2029706252
Cited by
91
References
156
Citations by year
2026: 2 · 2025: 4 · 2024: 1 · 2023: 3 · 2022: 1 · 2021: 5 · 2020: 1 · 2019: 5 · 2018: 4 · 2017: 6 · 2016: 2 · 2015: 5 · 2014: 6 · 2013: 1 · 2012: 3
FWCI
4.24
Type
journal article
Language
en
Open access
closed
Locations
  • Drug Safety (publishedVersion)
  • PubMed (publishedVersion)
  • UCL Discovery (University College London) (submittedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Coenzyme Q10 studies and effects
  • Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Lipids, and Metabolism
Keywords
statins, coenzyme Q10, myotoxicity, hepatotoxicity, statin adverse effects, cholesterol biosynthesis, mevalonate, statin dose, bioavailability
MeSH terms
Animals, Coenzymes, Humans, Kinetics, Ubiquinone, Hydroxymethylglutaryl-CoA Reductase Inhibitors

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