Mitochondrial cardiomyopathy and coenzyme Q10

Anna Gvozdjáková, M. Mikulecký, F. L. Crane, J. Kucharská, Germaine G Cornelissen-Guillaume, A. Kumar, P. Palacka, R. B. Singh

Research output: Contribution to journalArticlepeer-review

13 Scopus citations


Heart mitochondrial oxidative phosphorylation function and coenzyme Q10 (CoQ10) concentration in clinical and experimental cardiomyopathies are presented. In endomyocardial biopsies (EMB) of patients with cardiomyopathy of unknown etiology (CPUE), decreased mitochondrial respiration, ATP production and CoQ10 concentrations have been found. A positive relationship between the degree of rejection, decreased CoQ10 and OXPHOS function in EMB of transplanted hearts has been documented. In experimental medicine circadian and circasemidian rhythms of heart mitochondrial "CoQ10- CLOCK" have been found and different parameters of the cascade of oxidative phosphorylation between control and diabetic rats' hearts were estimated. Mapping changes in heart CoQ10 and ATP production along the 24-hour scale can help obtain a better understanding of triggers of acute heart attacks. A novel CoQ binding site in Voltage- Dependent Anion Channel (VDAC) of outer mitochondrial membrane is proposed [4]. CoQ10 targeted therapy of damaged mitochondria could be in the site of porin (VDAC) of the outer mitochondrial membrane where exogenous CoQ10 passes through this channel into mitochondria. Based on current knowledge, target of mitochondrial respiratory chain supplementary therapy with CoQ10 in cardiomyopathies is warranted.

Original languageEnglish (US)
Pages (from-to)29-46
Number of pages18
JournalWorld Heart Journal
Issue number1
StatePublished - Jan 2014


  • Chronobiology
  • Diabetes
  • Mitochondrial cardiomyopathy


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