Abnormal mitochondrial L-arginine transport contributes to the pathogenesis of heart failure and rexoygenation injury
Williams, David, Venardos, Kylie M., Byrne, Melissa, Joshi, Mandar, Horlock, Duncan, Lam, Nicholas T., Gregorevic, Paul, McGee, Sean L. and Kaye, David M. 2014, Abnormal mitochondrial L-arginine transport contributes to the pathogenesis of heart failure and rexoygenation injury, PLoS one, vol. 9, no. 8, Article number : e104643, pp. 1-11, doi: 10.1371/journal.pone.0104643.
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.
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