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Can coenzyme Q10 improve clinical and molecular parameters in fibromyalgia?

  • Mario D. Cordero*
  • , Elísabet Alcocer-Gómez
  • , Manuel De Miguel
  • , Ognjen Culic
  • , Angel M. Carrión
  • , José Miguel Alvarez-Suarez
  • , Pedro Bullón
  • , Maurizio Battino
  • , Ana Fernández-Rodríguez
  • , José Antonio Sánchez-Alcazar
  • *Corresponding author for this work
  • Facultad de Medicina, Universidad de Sevilla
  • University of Zagreb
  • Universidad Pablo de Olavide de Sevilla
  • Universita Politecnica Delle Marche
  • Universidad de Sevilla
  • Universidad Pablo de Olavide-CSIC-Junta de Andalucý́a

Research output: Contribution to journalReview articlepeer-review

80 Scopus citations

Abstract

Fibromyalgia (FM) is a complex disorder that affects up to 5% of the general population worldwide. Its pathophysiological mechanisms are difficult to identify and current drug therapies demonstrate limited effectiveness. Both mitochondrial dysfunction and coenzyme Q10 (CoQ10) deficiency have been implicated in FM pathophysiology. We have investigated the effect of CoQ10 supplementation. We carried out a randomized, double-blind, placebo-controlled trial to evaluate clinical and gene expression effects of forty days of CoQ10 supplementation (300 mg/day) on 20 FM patients. This study was registered with controlled-trials.com (ISRCTN 21164124). An important clinical improvement was evident after CoQ10 versus placebo treatment showing a reduction of FIQ (p<0.001), and a most prominent reduction in pain (p<0.001), fatigue, and morning tiredness (p<0.01) subscales from FIQ. Furthermore, we observed an important reduction in the pain visual scale (p<0.01) and a reduction in tender points (p<0.01), including recovery of inflammation, antioxidant enzymes, mitochondrial biogenesis, and AMPK gene expression levels, associated with phosphorylation of the AMPK activity. These results lead to the hypothesis that CoQ10 have a potential therapeutic effect in FM, and indicate new potential molecular targets for the therapy of this disease. AMPK could be implicated in the pathophysiology of FM. Antioxid. Redox Signal. 19, 1356-1361.

Original languageEnglish
Pages (from-to)1356-1361
Number of pages6
JournalAntioxidants and Redox Signaling
Volume19
Issue number12
DOIs
StatePublished - 20 Oct 2013
Externally publishedYes

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