Monoamine oxidase B prompts mitochondrial and cardiac dysfunction in pressure overloaded hearts.

@article{Kaludercic2014MonoamineOB,
  title={Monoamine oxidase B prompts mitochondrial and cardiac dysfunction in pressure overloaded hearts.},
  author={Nina Kaludercic and Andrea Carpi and Takahiro Nagayama and Vidhya Sivakumaran and Guangshuo Zhu and Edwin W. Lai and Djahida Bedja and Agnese De Mario and Kevin Chen and Kathleen L. Gabrielson and Merry L Lindsey and Karel Pacak and Eiki Takimoto and Jean Chen Shih and David A. Kass and Fabio di Lisa and Nazareno Paolocci},
  journal={Antioxidants & redox signaling},
  year={2014},
  volume={20 2},
  pages={267-80}
}
AIMS Monoamine oxidases (MAOs) are mitochondrial flavoenzymes responsible for neurotransmitter and biogenic amines catabolism. MAO-A contributes to heart failure progression via enhanced norepinephrine catabolism and oxidative stress. The potential pathogenetic role of the isoenzyme MAO-B in cardiac diseases is currently unknown. Moreover, it is has not been determined yet whether MAO activation can directly affect mitochondrial function. RESULTS In wild type mice, pressure overload induced… CONTINUE READING

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American journal of physiology. Heart and circulatory physiology • 2011
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