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Is inflammation a mitochondrial dysfunction-dependent event in Fibromyalgia?

Discussion in 'Fibromyalgia' started by Firestormm, Sep 11, 2012.

  1. Firestormm

    Firestormm Guest

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    Cornwall England
    Antioxid Redox Signal. 2012 Sep 3. [Epub ahead of print]: http://www.ncbi.nlm.nih.gov/pubmed/22938055
    Is inflammation a mitochondrial dysfunction-dependent event in Fibromyalgia?

    Cordero MD, Díaz-Parrado E, Carrión AM, Alfonsi S, Sánchez-Alcázar JA, Bullon P, Battino M, de Miguel M.
    Source

    Dpto. Citología e Histología Normal y Patológica, Facultad de Medicina. Universidad de Sevilla, 41009 Sevilla-Spain, Avda. Sánchez-Pizjuán s/n , Sevilla, Spain, 41009, +34 95 4551797 , +34 95 4551799; mdcormor@us.es.
    Abstract

    Fibromyalgia (FM) is a complex disorder that affects up to 5% of the general population worldwide. Both mitochondrial dysfunction and inflammation have been implicated in the pathophysiology of FM.

    We have investigated the possible relationship between mitochondrial dysfunction, oxidative stress and inflammation in FM.

    We studied thirty women diagnosed with FM and twenty healthy women. Blood mononuclear cells (BMCs) from FM patients showed reduced level of CoQ10, mtDNA contents, and high level of mitochondrial ROS, serum TNF-alpha 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 TNF-alpha levels (r = 0.791; P<0.001) were observed accompanied by a significant correlation of VAS with serum TNF-alpha 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 (BMCs) and in vivo (mice) CoQ10 deficiency model. Oral CoQ10 supplementation restored biochemical parameters and induced a significant improvement in clinical symptoms (P0.001).

    These results lead to the hypothesis that inflammation could be a mitochondrial dysfunction-dependent event implicated in the pathophysiology of FM in several patients indicating at mitochondria as a possible new therapeutic target.
     
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