doi:10.1016/j.mito.2016.06.007engYubero, D.Montero, R.Martín, M. A.Montoya, J.Ribes, A.Grazina, M.Trevisson, E.Rodriguez-Aguilera, J.Hargreaves, I. P.Salviati, L.Navas, P.Artuch, R.Jou, C.Jimenez-Mallebrera, C.Nascimento, A.Pérez-Dueñas, B.Ortez, C.Ramos, F.Colomer, J.O''Callaghan, M.Pineda, M.García-Cazorla, A.Espinós, C.Ruiz, A.Macaya, A.Marcé-Grau, A.Garcia-Villoria, J.Arias, A.Emperador, S.Ruiz-Pesini, E.Lopez-Gallardo, E.Neergheen, V.Simões, M.Diogo, L.Blázquez, A.González-Quintana, A.Delmiro, A.Domínguez-González, C.Arenas, J.García-Silva, M. T.Martín, E.Quijada, P.Hernández-Laín, A.Morán, M.Rivas Infante, E.Ávila Polo, R.Paradas Lópe, C.Bautista Lorite, J.Martínez Fernández, E. M.Cortés, A. B.Sánchez-Cuesta, A.Cascajo, M. V.Alcázar, M.Brea-Calvo, G.Secondary coenzyme Q10 deficiencies in oxidative phosphorylation (OXPHOS) and non-OXPHOS disordersART-2016-95666We evaluated the coenzyme Q10 (CoQ) levels in patients who were diagnosed with mitochondrial oxidative phosphorylation (OXPHOS) and non-OXPHOS disorders (n = 72). Data from the 72 cases in this study revealed that 44.4% of patients showed low CoQ concentrations in either their skeletal muscle or skin fibroblasts. Our findings suggest that secondary CoQ deficiency is a common finding in OXPHOS and non-OXPHOS disorders. We hypothesize that cases of CoQ deficiency associated with OXPHOS defects could be an adaptive mechanism to maintain a balanced OXPHOS, although the mechanisms explaining these deficiencies and the pathophysiological role of secondary CoQ deficiency deserves further investigation.2016http://zaguan.unizar.es/record/13056510.1016/j.mito.2016.06.007http://zaguan.unizar.es/record/130565oai:zaguan.unizar.es:130565MITOCHONDRION 30 (2016), 51-58All rights reservedhttp://www.europeana.eu/rights/rr-f/info:eu-repo/semantics/closedAccess