Identificador persistente para citar o vincular este elemento: http://hdl.handle.net/10553/43004
Título: Antioxidants can inhibit basal autophagy and enhance neurodegeneration in models of polyglutamine disease
Autores/as: Underwood, Benjamin R.
Imarisio, Sara
Fleming, Angeleen
Rose, Claudia
Krishna, Gauri
Heard, Phoebe
Quick, Marie
Korolchuk, Viktor I.
Renna, Maurizio
Sarkar, Sovan
Garcia-Arencibia, Moises 
O'Kane, Cahir J.
Murphy, Michael P.
Rubinsztein, David C.
Clasificación UNESCO: 320507 Neurología
Palabras clave: Antioxidants
Autophagy
Zebrafish
Polyglutamine
Fecha de publicación: 2010
Editor/a: 0964-6906
Publicación seriada: Human Molecular Genetics 
Resumen: Many neurodegenerative diseases exhibit protein accumulation and increased oxidative stress. Therapeutic strategies include clearing aggregate-prone proteins by enhancing autophagy or decreasing oxidative stress with antioxidants. Many autophagy-inducing stimuli increase reactive oxygen species (ROS), raising concerns that the benefits of autophagy up-regulation may be counterbalanced by ROS toxicity. Here we show that not all autophagy inducers significantly increase ROS. However, many antioxidants inhibit both basal and induced autophagy. By blocking autophagy, antioxidant drugs can increase the levels of aggregate-prone proteins associated with neurodegenerative disease. In fly and zebrafish models of Huntington's disease, antioxidants exacerbate the disease phenotype and abrogate the rescue seen with autophagy-inducing agents. Thus, the potential benefits in neurodegenerative diseases of some classes of antioxidants may be compromised by their autophagy-blocking properties.
URI: http://hdl.handle.net/10553/43004
ISSN: 0964-6906
DOI: 10.1093/hmg/ddq253
WOS:000280704800011
Fuente: Human Molecular Genetics [ISSN 0964-6906], v. 19 (17), p. 3413-3429
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