期刊
ANTIOXIDANTS & REDOX SIGNALING
卷 20, 期 8, 页码 1169-1180出版社
MARY ANN LIEBERT, INC
DOI: 10.1089/ars.2013.5198
关键词
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资金
- Fondo Europeo de Desarrollo Regional (FEDER-Union Europea) [FIS PI10/00543]
- Servicio Andaluz de Salud-Junta de Andalucia [SAS 111242]
- Proyecto de Investigacion de Excelencia de la Junta de Andalucia [CTS-5725]
- Federacion Andaluza de Fibromialgia y Fatiga Cronica (ALBA Andalucia)
- FOICAM (Spanish research association)
Aims: Fibromyalgia (FM) is a prevalent chronic pain syndrome characterized by generalized hyperalgesia associated with a wide spectrum of symptoms such as fatigue and joint stiffness. Diagnosis of FM is difficult due to the lack of reliable diagnostic biomarkers, while treatment is largely inadequate. We have investigated the role of coenzyme Q(10) (CoQ(10)) deficiency and mitochondrial dysfunction in inflammasome activation in blood cells from FM patients, and in vitro and in vivo CoQ(10) deficiency models. Results: Mitochondrial dysfunction was accompanied by increased protein expression of interleukin (IL)-1, NLRP3 (NOD-like receptor family, pyrin domain containing 3) and caspase-1 activation, and an increase of serum levels of proinflammatory cytokines (IL-1 and IL-18). CoQ(10) deficiency induced by p-aminobenzoate treatment in blood mononuclear cells and mice showed NLRP3 inflammasome activation with marked algesia. A placebo-controlled trial of CoQ(10) in FM patients has shown a reduced NLRP3 inflammasome activation and IL-1 and IL-18 serum levels. Innovation: These results show an important role for the NLRP3 inflammasome in the pathogenesis of FM, and the capacity of CoQ10 in the control of inflammasome. Conclusion: These findings provide new insights into the pathogenesis of FM and suggest that NLRP3 inflammasome inhibition represents a new therapeutic intervention for the disease. Antioxid. Redox Signal. 20, 1169-1180.
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