Abnormal Mitochondrial L-Arginine Transport Contributes to the Pathogenesis of Heart Failure and Rexoygenation Injury
David Williams, Kylie M Venardos, Melissa Byrne, Mandar Joshi, Duncan Horlock, Nicholas T Lam, Paul Gregorevic, Sean L McGee, David M Kaye
PLOS ONE | PUBLIC LIBRARY SCIENCE | Published : 2014
BACKGROUND: 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. METHODS AND RESULTS: In mito..View full abstract
Awarded by NHMRC
Funding provided by NHMRC Program Grant 1036352. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.