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Fibromyalgia Research Studies

Fibromyalgia Research Studies

The following is a list of Fibromyalgia research studies:

1.  Cordero, M. D., de Miguel, M., Carmona-López, I., Bonal, P., Campa, F., & Moreno-Fernández, A. M. (2010). Oxidative stress and mitochondrial dysfunction in fibromyalgia. Neuroendocrinology Letters, 31(2). Abstract conclusion: Coenzyme Q10 (CoQ10) deficiency, an essential electron carrier in the mitochondrial respiratory chain and a strong antioxidant, alters mitochondria function and mitochondrial respiratory complexes organization and leading to increased ROS generation. Recently have been showed CoQ10 deficiency in blood mononuclear cells in FM patients, so if the hypothesis that mitochondrial dysfunction is the origin of oxidative stress in FM patients is demonstrated, could help to understand the complex pathophysiology of this disorder and may lead to development of new therapeutic strategies for prevention and treatment of this disease.

2.  Cordero, M. D., De Miguel, M., Fernández, A. M. M., López, I. M. C., Garrido, J., Navas, P., & Alcázar, J. A. S. (2010). Research article Mitochondrial dysfunction and mitophagy activation in blood mononuclear cells of fibromyalgia patients: implications in the pathogenesis of the disease. Arthritis Res Ther, 12(1), R17. Abstract conclusion: 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. These findings may support the role of oxidative stress and mitophagy in the pathophysiology of fibromyalgia.

3.  Cordero, M. D., Moreno-Fernández, A. M., Bonal, P., Campa, F., Jiménez-Jiménez, L. M., Ruiz-Losada, A., ... & Navas, P. (2009). Coenzyme Q10 distribution in blood is altered in patients with fibromyalgia. Clinical biochemistry, 42(7), 732-735. Abstract conclusion: The distribution of CoQ(10) in blood components was altered in FM patients. Also, our results confirm the oxidative stress background of this disease probably due to a defect on the distribution and metabolism of CoQ(10) in cells and tissues. The protection caused in mononuclear cells by CoQ(10) would indicate the benefit of its supplementation in FM patients.

4.  Pieczenik, S. R., & Neustadt, J. (2007). Mitochondrial dysfunction and molecular pathways of disease. Experimental and molecular pathology, 83(1), 84-92. Abstract conclusion: Antioxidant therapies hold promise for improving mitochondrial performance. Physicians seeking systematic treatments for their patients might consider testing urinary organic acids to determine how best to treat them. If in the next 50 years advances in mitochondrial treatments match the immense increase in knowledge about mitochondrial function that has occurred in the last 50 years, mitochondrial diseases and dysfunction will largely be a medical triumph.

5.  Cordero, M. D., Díaz-Parrado, E., Carrión, A. M., Alfonsi, S., Sánchez-Alcazar, J. A., Bullón, P., ... & de Miguel, M. (2013). Is inflammation a mitochondrial dysfunction-dependent event in fibromyalgia? Antioxidants & redox signaling, 18(7), 800-807. Abstract conclusion: 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.

6.  Cordero, M. D., de Miguel, M., & Moreno-Fernandez, A. M. (2011). Mitochondrial dysfunction in fibromyalgia and its implication in the pathogenesis of disease. Medicina clinica, 136(6), 252-256. Abstract conclusion: Fibromyalgia (FM) is a chronic pain syndrome with unknown etiology. Recent studies have shown evidence demonstrating that oxidative stress may have a role in the pathophysiology of FM, however it is still not clear whether oxidative stress is the cause or the effect of the abnormalities documented in FM. Furthermore, it is also controversial the role of mitochondria in the pathophysiology of FM, however signs associated with mitochondrial dysfunction have been observed in FM. Mitochondria are also known to be strong producers of ROS, so have been related with the pathogenic mechanism of numerous diseases including FM. To this respect, it has been observed antioxidants therapies might be beneficial to improve the mitochondrial performance. Therefore, the dysfunction mitochondrial opens a great field of therapeutic research, for what it should start considering in the clinical medicine the boarding of the FM by means of therapy with antioxidant and drugs related to the mitochondrial biogenesis.

 
 
 
 
 

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