Statin-induced mitochondrial dysfunction and targeting coenzyme Q10 therapy

Anna Gvozdjáková, J. Kucharská, R. B. Singh, O. Vančová, O. Uličná, V. Mojto, J. Fedačko, D. Pella, N. S. Verma, Germaine G Cornelissen-Guillaume

Research output: Contribution to journalArticlepeer-review

8 Scopus citations


Statins, inhibitors of 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMG-CoA reductase) decrease LDLcholesterol, triacylglycerols, coenzyme Q10 (CoQ10) concentrations and isoprenoids synthesis. Benefits of statins include vasodilatatory, antiarrhythmic, antitrombotic and antiinflammatory effects (pleiotropic), stimulation of endogenous antioxidants function and reduction of oxidative stress. Decreased CoQ10 concentration is an important reason for the occurrence of adverse effects, as statin-induced myopathy. In hypercholesterolemic rats treated with atorvastatin (dose 80 mg/(kg body weight)/day) for four weeks, we documented dysfunction of myocardium and liver mitochondrial oxidative phosphorylation, and a decrease in mitochondrial CoQ9-OX and CoQ10-OX concentrations. Reduction of CoQ10 concentrations and dysfunction of skeletal muscle mitochondrial respiration and ATP production brought about by statin use can be referred to as “statin-induced mitochondrial myopathy”. From our experience and that of several other authors, targeting reduction of the statin-induced mitochondrial myopathy is appropriate at daily doses of 60 mg-100 to 200 mg CoQ10, in particular for patients with muscle pain, general weakness, increased activity of creatine kinase and transaminases, in cardiovascular diseases, impairment of memory, and sexual dysfunction.

Original languageEnglish (US)
Pages (from-to)171-182
Number of pages12
JournalWorld Heart Journal
Issue number2
StatePublished - 2016

Bibliographical note

Funding Information:
Supported by Grants VEGA 1/0328/10, 1/0614/12.

Publisher Copyright:
© 2016 Nova Science Publishers, Inc.


  • Coenzyme Q
  • Mitochondrial myopathy
  • Statins


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