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Updated: May 12, 2026
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Evaluating the Role of Mitochondrial Function in Cancer-related Fatigue
Published on: May 17, 2018
Could mitochondrial dysfunction be a differentiating marker between chronic fatigue syndrome and fibromyalgia?
Jesús Castro-Marrero1, Mario D Cordero, Naia Sáez-Francas
11 CFS Unit, Institut de Recerca Vall d'Hebron, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona , Barcelona, Spain .
Antioxidants & Redox Signaling
|April 23, 2013
Summary
Mitochondrial dysfunction, marked by low Coenzyme Q10 and ATP, is evident in Chronic Fatigue Syndrome (CFS) and Fibromyalgia (FM). Oxidative stress and differing mitochondrial markers suggest mitochondria as a therapeutic target for these conditions.
Area of Science:
- Biochemistry
- Cell Biology
- Medical Science
Background:
- Chronic Fatigue Syndrome (CFS) and Fibromyalgia (FM) are prevalent, complex illnesses with unknown etiology.
- Emerging research implicates mitochondrial dysfunction in the pathophysiology of both CFS and FM.
- Investigating mitochondrial biogenesis and oxidative stress may reveal key differences and therapeutic targets.
Purpose of the Study:
- To investigate the association between mitochondrial biogenesis and oxidative stress in patients with CFS and FM.
- To explore potential differences in mitochondrial function between CFS and FM patients.
- To identify mitochondria as a potential therapeutic target for CFS and FM.
Main Methods:
- Peripheral blood mononuclear cells from 23 CFS patients, 20 FM patients, and 15 healthy controls were analyzed.
- Levels of Coenzyme Q10, ATP, and lipid peroxidation were measured.
- Mitochondrial citrate synthase activity, mtDNA/gDNA ratio, and key mitochondrial gene expression were assessed.
Main Results:
- CFS and FM patients exhibited decreased Coenzyme Q10 and ATP levels compared to controls.
- Elevated lipid peroxidation in CFS/FM patients indicated oxidative stress-induced damage.
- FM patients showed reduced mitochondrial citrate synthase activity, mtDNA content, and key gene expression, unlike CFS patients.
Conclusions:
- Mitochondrial dysfunction is a significant factor in both CFS and FM, evidenced by reduced energy production and increased oxidative stress.
- Distinct patterns of mitochondrial dysfunction may serve as markers to differentiate between CFS and FM.
- Targeting mitochondrial pathways presents a promising therapeutic strategy for managing CFS and FM.
