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Mitochondrial dysfunction and mitophagy activation in blood mononuclear cells in fibromyalgia

 

 



Arthritis Res Ther. 2010 Jan 28;12(1):R17. [Epub ahead of print]


Mitochondrial dysfunction and mitophagy activation in blood mononuclear cells of fibromyalgia patients: implication in the pathogenesis of the disease.

Cordero MD, De Miguel M, Moreno Fernandez AM, Carmona Lopez IM, Garrido Maraver J, Cotan D, Gomez Izquierdo L, Bonal P, Campa F, Bullon P, Navas P, Sanchez Alcazar JA.



INTRODUCTION: Fibromyalgia is a chronic pain syndrome with unknown etiology. Recent studies have shown some evidence demonstrating that oxidative stress may have a role in the pathophysiology of fibromyalgia. However, it is still not clear whether oxidative stress is the cause or the effect of the abnormalities documented in fibromyalgia. Furthermore, the role of mitochondria in the redox imbalance reported in fibromyalgia is also controversial. We undertook this study to investigate the role of mitochondrial dysfunction, oxidative stress and mitophagy in fibromyalgia.

METHODS: We studied 20 patients (2 males and 18 females) recruited from the database of the Sevillian Fibromyalgia Association and 10 healthy controls. We evaluated mitochondrial function in blood mononuclear cells from fibromyalgia patients measuring coenzyme Q10 levels by high performance liquid chromatography (HPLC), and mitochondrial membrane potential by flow cytometry. Oxidative stress was determined by measuring mitochondrial superoxide production by MitoSOXTM, and lipid peroxidation in blood mononuclear cells and plasma from fibromyalgia patients. Autophagy activation was evaluated by quantifying the fluorescence intensity of LysoTrackerTM Red staining of blood mononuclear cells. Mitophagy was confirmed by measuring citrate synthase activity and electron microscopy examination of blood mononuclear cells.

RESULTS: We found reduced levels of coenzyme Q10, decreased mitochondrial membrane potential, increased level of mitochondrial superoxide in blood mononuclear cells, and increased levels of lipid peroxidation in both blood mononuclear cells and plasma from fibromyalgia patients. Mitochondrial dysfunction was also associated with increased expression of autophagic genes and the elimination of dysfunctional mitochondria by mitophagy.

CONCLUSIONS: These findings may support the role of oxidative stress and mitophagy in the pathophysiology of fibromyalgia.


PMID: 20109177 [PubMed - as supplied by publisher]

 

 

 

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