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Mitochondrial dysfunction and ROS induce inflammation in Fibromyalgia patients

AutorCordero, Mario D. ; Alcocer-Gómez, Elísabet; Díaz-Parrado, Eduardo; Carrión Rodríguez, Ángel Manuel ; Alfonsi, Simona; Sánchez-Alcázar, José Antonio ; Miguel, Manuel de
Fecha de publicación2012
Citación22nd IUBMB and 37th FEBS (2012)
Resumen[Objective]: Mitochondrial dysfunction has been implicated in the pathophysiology of Fibromyalgia (FM). Inflammation has been also hypothesized in FM. We will study the possible relationship relationship between mitochondrial dysfunction, oxidative stress and inflammation in FM. [Methods]: Mitochondrial dysfunction was studied assaying Coenzyme Q10 (CoQ10), mitochondrial ROS production and mtDNA contents in blood mononuclear cells (BMCs). Serum TNF-alphaand gene expressionwas assayed as inflammatory mediator in patients. Clinical symptoms were evaluated using Visual Analogical Scale of pain (VAS), and Fibromyalgia Impact Questionnaire (FIQ). CoQ10 deficiency was induced in healthy cells and mice to evaluate TNF-alpha release. [Results]: BMCs from FM patients showed reduced level of CoQ10, mtDNA, and high level of mitochondrial ROS and TNFalpha serum and transcript levels. A significant negative correlation between CoQ10 and TNF-alpha levels (r = )0.588; p < 0.01), and a positive correlation between ROS and TNFalpha levels (r = 0.791; p < 0.001) were observed accompanied by significant correlation of VAS with TNF-alpha serum and transcript levels (r = 0.4507; p < 0.05 and r = 0.7089; p < 0.001, respectively). TNF-alpha release was observed in an in vitro and in vivo CoQ10 deficiency model. Conclusions: Our data evidence that mitochondrial dysfunction has an important role in FM. Inflammation is a mitochondrial dysfunction-depended event implicated in the pathophysiology of FM.
DescripciónResumen del póster presentado al 22nd IUBMB & 37th FEBS Congress, celebrado en Sevilla (España) del 4 al 9 de septiembre de 2012.
URIhttp://hdl.handle.net/10261/130132
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