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Successful reversal of propionic acidaemia associated cardiomyopathy: evidence for low myocardial coenzyme Q10 status and secondary mitochondrial dysfunction as an underlying pathophysiological mechanism.

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第一作者： J,Baruteau

第一单位： Metabolic Medicine Department, Great Ormond Street Hospital, London, UK. Electronic address: jbaruteau@yahoo.fr.

作者： J,Baruteau ^[1] ; I,Hargreaves ^[2] ; S,Krywawych ^[3] ; A,Chalasani ^[2] ; J M,Land ^[2] ; J E,Davison ^[4] ; M K,Kwok ^[4] ; G,Christov ^[5] ; A,Karimova ^[5] ; M,Ashworth ^[6] ; G,Anderson ^[6] ; H,Prunty ^[3] ; S,Rahman ^[7] ; S,Grünewald ^[7]

作者单位： Metabolic Medicine Department, Great Ormond Street Hospital, London, UK. Electronic address: jbaruteau@yahoo.fr. ^[1] Neurometabolic Laboratory, National Hospital for Neurology and Neurosurgery, London, UK. ^[2] Chemical Pathology, Great Ormond Street Hospital, London, UK. ^[3] Metabolic Medicine Department, Great Ormond Street Hospital, London, UK. ^[4] Cardiothoracic Unit, Great Ormond Street Hospital, London, UK. ^[5] Pathology Laboratory, Great Ormond Street Hospital, London, UK. ^[6] Metabolic Medicine Department, Great Ormond Street Hospital, London, UK; Clinical and Molecular Genetics Unit, UCL Institute of Child Health, London, UK. ^[7]

关键词 Cardiomyopathy Coenzyme Q10 Inborn metabolic disease Propionic acidaemia Respiratory chain Ubiquinone