Cardiovasc Res (2011) 90 (2): 276-284. doi: 10.1093/cvr/cvq376
Ana Planavila1,2,*, Roser Iglesias1,2, Marta Giralt1,2 and Francesc Villarroya1,2
1Departament de Bioquímica i Biologia Molecular, Institut de Biomedicina de la Universitat de Barcelona (IBUB), Universitat de Barcelona, Avda Diagonal 645, Barcelona E-08028, Spain
2CIBER Fisiopatología de la Obesidad y Nutrición (CIBEROBN), Barcelona, Spain
"Collectively, these findings reveal a major involvement of the Sirt1–PPARα interaction in the protective role of Sirt1 against cardiac hypertrophy."
Monday, April 18, 2011
Friedreich's ataxia: Past, present and future
doi:10.1016/j.brainresrev.2011.04.001
Daniele Marmolino,
Laboratoire de Neurologie experimentale, Universite Libre de Bruxeles (ULB), Route de Lennik 808, Campus Erasme - 1070 Bruxelles, Belgium
Keywords: Friedreich's ataxia; Frataxin; GAA; Iron; Fe-S clusters; Oxidative stress; FRDA pathogenesis; frataxin function; new treatments; animal and cellular models.
Daniele Marmolino,
Laboratoire de Neurologie experimentale, Universite Libre de Bruxeles (ULB), Route de Lennik 808, Campus Erasme - 1070 Bruxelles, Belgium
Keywords: Friedreich's ataxia; Frataxin; GAA; Iron; Fe-S clusters; Oxidative stress; FRDA pathogenesis; frataxin function; new treatments; animal and cellular models.
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