Mitochondrial dysfunction in antiphospholipid syndrome: implications in the pathogenesis of the disease and effects of coenzyme Q(10) treatment.

@article{PrezSnchez2012MitochondrialDI,
  title={Mitochondrial dysfunction in antiphospholipid syndrome: implications in the pathogenesis of the disease and effects of coenzyme Q(10) treatment.},
  author={Carlos P{\'e}rez-S{\'a}nchez and Patricia Ruiz-Limon and Mar{\'i}a {\'A}ngeles Aguirre and Maria Laura Bertolaccini and Munther A. Khamashta and Antonio Rodriguez-Ariza and Pedro Segui and Eduardo Collantes-Estevez and Nuria Barbarroja and Husam Khraiwesh and Jos{\'e} Antonio Gonz{\'a}lez-Reyes and J. M. Villalba and Francisco Velasco and Mar{\'i}a Jos{\'e} Cuadrado and Chary L{\'o}pez-Pedrera},
  journal={Blood},
  year={2012},
  volume={119 24},
  pages={5859-70}
}
The exact mechanisms underlying the role of oxidative stress in the pathogenesis and the prothrombotic or proinflammatory status of antiphospholipid syndrome (APS) remain unknown. Here, we investigate the role of oxidative stress and mitochondrial dysfunction in the proatherothrombotic status of APS patients induced by IgG-antiphospholipid antibodies and the beneficial effects of supplementing cells with coenzyme Q(10) (CoQ(10)). A significant increase in relevant prothrombotic and inflammatory… CONTINUE READING
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