Cordero 2013 Antioxid Redox Signal
Cordero MD, DΓaz-Parrado E, CarriΓ³n AM, Alfonsi S, SΓ‘nchez-Alcazar JA, BullΓ³n P, Battino M, de Miguel M (2013) Is inflammation a mitochondrial dysfunction-dependent event in fibromyalgia? Antioxid Redox Signal 18:800-7. |
Cordero MD, Diaz-Parrado E, Carrion AM, Alfonsi S, Sanchez-Alcazar JA, Bullon P, Battino M, de Miguel M (2013) Antioxid Redox Signal
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 30 women diagnosed with FM and 20 healthy women. Blood mononuclear cells (BMCs) from FM patients showed reduced level of coenzyme Qββ (CoQββ) and mtDNA contents and high level of mitochondrial reactive oxygen species (ROS) and serum tumor necrosis factor (TNF)-alpha and transcript levels. A significant negative correlation between CoQββ 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 visual analogical scale 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) CoQββ deficiency model. Oral CoQββ 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.
Labels: MiParea: mtDNA;mt-genetics, Patients
Pathology: Other
Organism: Mouse