Progressive mitochondrial protein lysine acetylation and heart failure in a model of Friedreich’s ataxia cardiomyopathy

@inproceedings{Stram2017ProgressiveMP,
  title={Progressive mitochondrial protein lysine acetylation and heart failure in a model of Friedreich’s ataxia cardiomyopathy},
  author={Amanda R Stram and Gregory R. Wagner and Brian D. Fogler and P. Melanie Pride and Matthew D Hirschey and Ronald M Payne},
  booktitle={PloS one},
  year={2017}
}
INTRODUCTION The childhood heart disease of Friedreich's Ataxia (FRDA) is characterized by hypertrophy and failure. It is caused by loss of frataxin (FXN), a mitochondrial protein involved in energy homeostasis. FRDA model hearts have increased mitochondrial protein acetylation and impaired sirtuin 3 (SIRT3) deacetylase activity. Protein acetylation is an important regulator of cardiac metabolism and loss of SIRT3 increases susceptibility of the heart to stress-induced cardiac hypertrophy and… CONTINUE READING