p53-PGC-1α pathway mediates oxidative mitochondrial damage and cardiomyocyte necrosis induced by monoamine oxidase-A upregulation: role in chronic left ventricular dysfunction in mice.

@article{Villeneuve2013p53PGC1PM,
  title={p53-PGC-1α pathway mediates oxidative mitochondrial damage and cardiomyocyte necrosis induced by monoamine oxidase-A upregulation: role in chronic left ventricular dysfunction in mice.},
  author={Christelle Villeneuve and C{\'e}line Guilbeau-Frugier and Pierre Sicard and Olivier Lairez and Catherine Ordener and Thibaut Duparc and Damien de Paulis and Bettina Couderc and Odile Spreux-Varoquaux and Florence Tortosa and Anne Garnier and Claude Knauf and Philippe Valet and Elisabetta Borchi and Chiara Nediani and Abdallah Gharib and Michel Ovize and Marie-Bernadette Delisle and Angelo Parini and Jeanne Mialet-Perez},
  journal={Antioxidants & redox signaling},
  year={2013},
  volume={18 1},
  pages={5-18}
}
AIMS Oxidative stress and mitochondrial dysfunction participate together in the development of heart failure (HF). mRNA levels of monoamine oxidase-A (MAO-A), a mitochondrial enzyme that produces hydrogen peroxide (H(2)O(2)), increase in several models of cardiomyopathies. Therefore, we hypothesized that an increase in cardiac MAO-A could cause oxidative stress and mitochondrial damage, leading to cardiac dysfunction. In the present study, we evaluated the consequences of cardiac MAO-A… CONTINUE READING
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