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Related Experiment Video

Updated: May 19, 2026

Phosphorus-31 Magnetic Resonance Spectroscopy: A Tool for Measuring In Vivo Mitochondrial Oxidative Phosphorylation Capacity in Human Skeletal Muscle
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Is inflammation a mitochondrial dysfunction-dependent event in fibromyalgia?

Mario D Cordero1, Eduardo Díaz-Parrado, Angel M Carrión

  • 1Dpto. Citología e Histología Normal y Patológica, Facultad de Medicina, Universidad de Sevilla, Spain. mdcormor@us.es

Antioxidants & Redox Signaling
|September 4, 2012
PubMed
Summary

Fibromyalgia patients exhibit mitochondrial dysfunction, increased oxidative stress, and inflammation. Coenzyme Q10 (CoQ10) supplementation improved symptoms, suggesting mitochondria are a therapeutic target for fibromyalgia.

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Area of Science:

  • Biochemistry
  • Immunology
  • Cell Biology

Background:

  • Fibromyalgia (FM) affects up to 5% globally, with mitochondrial dysfunction and inflammation implicated in its pathophysiology.
  • Investigating the interplay between mitochondrial dysfunction, oxidative stress, and inflammation in FM is crucial for understanding disease mechanisms.

Purpose of the Study:

  • To explore the relationship between mitochondrial dysfunction, oxidative stress, and inflammation in fibromyalgia patients.
  • To assess the therapeutic potential of coenzyme Q10 (CoQ10) in managing FM symptoms.

Main Methods:

  • Comparative analysis of blood mononuclear cells (BMCs) and serum from 30 FM patients and 20 healthy controls.
  • Measurement of coenzyme Q10 (CoQ10), mitochondrial DNA (mtDNA), reactive oxygen species (ROS), and tumor necrosis factor-alpha (TNF-alpha).
  • In vitro and in vivo models of CoQ10 deficiency, followed by oral CoQ10 supplementation in FM patients.

Main Results:

  • FM patients displayed reduced CoQ10 and mtDNA levels, elevated mitochondrial ROS, and increased serum TNF-alpha.
  • Significant negative correlation between CoQ10 and TNF-alpha; positive correlation between ROS and TNF-alpha.
  • Oral CoQ10 supplementation normalized biochemical markers and significantly improved clinical fibromyalgia symptoms.

Conclusions:

  • Inflammation in FM may be a consequence of mitochondrial dysfunction, highlighting mitochondria as a potential therapeutic target.
  • Coenzyme Q10 (CoQ10) supplementation demonstrates efficacy in improving biochemical and clinical outcomes in fibromyalgia.
  • Targeting mitochondrial dysfunction offers a promising therapeutic strategy for fibromyalgia management.