Abnormal mitochondrial L-arginine transport contributes to the pathogenesis of heart failure and rexoygenation injury
Data(s) |
11/08/2014
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Resumo |
Impaired mitochondrial function is fundamental feature of heart failure (HF) and myocardial ischemia. In addition to the effects of heightened oxidative stress, altered nitric oxide (NO) metabolism, generated by a mitochondrial NO synthase, has also been proposed to impact upon mitochondrial function. However, the mechanism responsible for arginine transport into mitochondria and the effect of HF on such a process is unknown. We therefore aimed to characterize mitochondrial L-arginine transport and to investigate the hypothesis that impaired mitochondrial L-arginine transport plays a key role in the pathogenesis of heart failure and myocardial injury. |
Identificador | |
Idioma(s) |
eng |
Publicador |
Public Library of Science |
Relação |
http://dro.deakin.edu.au/eserv/DU:30067306/venardos-abnormal-2014.pdf http://www.dx.doi.org/10.1371/journal.pone.0104643 http://www.ncbi.nlm.nih.gov/pubmed/25111602 |
Direitos |
2014, Public Library of Science |
Palavras-Chave | #Science & Technology #Multidisciplinary Sciences #Science & Technology - Other Topics #NITRIC-OXIDE SYNTHASE #ISCHEMIA-REPERFUSION INJURY #ISOLATED CARDIAC MITOCHONDRIA #MYOCARDIAL-ISCHEMIA #COMPLEX-I #ENDOTHELIAL-CELLS #METABOLIC STATES #AMINO-ACIDS #MODULATION #BIOGENESIS |
Tipo |
Journal Article |