Related Experiment Video
Updated: Feb 27, 2026
Procoagulant Platelet Characterization by Measuring Phosphatidylserine Exposure and Microvesicle Release from Human Purified Platelets
Published on: November 29, 2024
Ubiquinol Effects on Antiphospholipid Syndrome Prothrombotic Profile: A Randomized, Placebo-Controlled Trial
Carlos Pérez-Sánchez1, María Ángeles Aguirre1, Patricia Ruiz-Limón1
1From the Instituto Maimónides de Investigación Biomédica de Córdoba, Córdoba, Spain (C.P.-S., M.Á.A., P.R.-L., M.C.A.-A., Y.J.-G., I.A.-d.l.R., A.R.A., P.S., E.C.-E., N.B., F.V., C.L.-P.); Unidad de Gestión Clínica Reumatología (M.Á.A., E.C.-E., C.L.-P.), Unidad de Gestión Clínica Radiología (P.S.), and Unidad de Gestión Clínica Hematología (F.V.), Hospital Universitario Reina Sofía, Córdoba, Spain; Departamento de Biología Celular, Fisiología e Inmunología, Campus de Excelencia Internacional Agroalimentario, ceiA3 (L.F.-d.R., J.A.G.-R., J.M.V.) and Departamento de Medicina (Medicina, Dermatología y Otorrinolaringología) (E.C.-E.), Universidad de Córdoba, Córdoba, Spain; Lupus Research Unit, Hospital St Thomas, London, United Kingdom (M.J.C.); and Center of Research of Immunopathology and Rare Diseases-Coordinating Center of Piemonte and Valle d'Aosta Network for Rare Diseases, University of Turin, Italy (S.S., I.C.).
Objective:
Antiphospholipid syndrome (APS) leukocytes exhibit an oxidative perturbation, directly linked to alterations in mitochondrial dynamics and metabolism. This disturbance is related to the patients' prothrombotic status and can be prevented by in vitro treatment with coenzyme Q10. Our aim was to investigate short-term effects of in vivo ubiquinol (reduced coenzyme Q10 [Qred]) supplementation on markers related to inflammation and thrombosis in APS through a prospective, randomized, crossover, placebo-controlled trial.
Approach And Results:
Thirty-six patients with APS were randomized to receive Qred (200 mg/d) or placebo for 1 month. Thirty-three patients with APS completed the intervention, which increased plasma coenzyme Q10. Qred improved endothelial function and decreased monocyte expression of prothrombotic and proinflammatory mediators, inhibited phosphorylation of thrombosis-related protein kinases, and decreased peroxides and percentage of monocytes with depolarized mitochondria; mitochondrial size was increased, and mitochondrial biogenesis-related genes were upregulated. Qred ameliorated extruded neutrophil extracellular traps in neutrophils and downregulated peroxides, intracellular elastase, and myeloperoxidase. Nanostring microRNA profiling revealed 20 microRNAs reduced in APS monocytes, and 16 of them, with a preponderance of cardiovascular disease-related target mRNAs, were upregulated. Monocytes gene profiling showed differential expression of 29 atherosclerosis-related genes, 23 of them changed by Qred. Interaction networks of genes and microRNAs were identified. Correlation studies demonstrated co-ordinated effects of Qred on thrombosis and endothelial function-associated molecules.
Conclusions:
Our results highlight the potential of Qred to modulate the overexpression of inflammatory and thrombotic risk markers in APS. Because of the absence of clinically significant side effects and its potential therapeutic benefits, Qred might act as safe adjunct to standard therapies in APS.
Clinical Trial Registration:
URL: http://www.clinicaltrials.gov. Unique identifier: NCT02218476.
