RT Journal Article
T1 Mitochondrial dysfunction and mitophagy activation in blood mononuclear cells of fibromyalgia patients: implications in the pathogenesis of the disease.
A1 Cordero, Mario D.
A1 De Miguel, Manuel
A1 Moreno Fernández, Ana M.
A1 Carmona López, Inés M.
A1 Garrido Maraver, Juan
A1 Cotán, David.
A1 Gómez-Izquierdo, Lourdes
A1 Bonal, Pablo
A1 Campa, Francisco
A1 Bullon, Pedro
A1 Navas, Plácido
A1 Sánchez Alcázar, José A.
K1 Mitocondrias
K1 Fibromialgia
K1 Leucocitos Mononucleares
AB 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 also is controversial. We undertook this study to investigate the role of mitochondrial dysfunction, oxidative stress, and mitophagy in fibromyalgia. Methods. We studied 20 patients (2 male, 18 female patients) 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 with high-performance liquid chromatography (HPLC), and mitochondrial membrane potential with flow cytometry. Oxidative stress was determined by measuring mitochondrial superoxide production with MitoSOX™ and lipid peroxidation in blood mononuclear cells and plasma from fibromyalgia patients. Autophagy activation was evaluated by quantifying the fluorescence intensity of LysoTracker™ 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 levels 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 with mitophagy. Conclusions. These findings may support the role of oxidative stress and mitophagy in the pathophysiology of fibromyalgia.
PB BioMed Central
YR 2010
FD 2010-01-28
LK http://hdl.handle.net/10668/376
UL http://hdl.handle.net/10668/376
LA en
NO Cordero MD, De Miguel M, Moreno Fernández AM, Carmona López IM, Garrido Maraver J,  Cotán D, et al. Mitochondrial dysfunction and mitophagy activation in blood mononuclear cells of fibromyalgia patients: implications in the pathogenesis of the disease. Arthritis Res Ther. 2010;12(1):R17
DS RISalud
RD Apr 11, 2025