Biomolecules damage and redox status abnormalities in Fabry patients before and during enzyme replacement therapy.

@article{Biancini2016BiomoleculesDA,
  title={Biomolecules damage and redox status abnormalities in Fabry patients before and during enzyme replacement therapy.},
  author={Giovana Brondani Biancini and Carlos Eduardo Diaz Jacques and Tatiane Grazieli Hammerschmidt and Heryk Motta de Souza and Bruna Donida and Marion Deon and Filippo Pinto e Vairo and Charles M Lourenço and Roberto Giugliani and Carmen Regla Vargas},
  journal={Clinica chimica acta; international journal of clinical chemistry},
  year={2016},
  volume={461},
  pages={41-6}
}
Fabry disease (FD) is caused by deficient activity of the lysosomal enzyme α-galactosidase A. Its substrates, mainly globotriaosylceramide (Gb3), accumulate and seem to induce other pathophysiological findings of FD. Once enzyme replacement therapy (ERT) is not completely efficient on preventing disease progress in FD patients, elucidating the underlying mechanisms in FD pathophysiology is essential to the development of additional therapeutic strategies. We investigated 58 Fabry patients (23… CONTINUE READING

Similar Papers

Loading similar papers…