Role of calcineurin in neurodegeneration produced by misfolded proteins and endoplasmic reticulum stress.
Curr Opin Cell Biol
; 23(2): 223-30, 2011 Apr.
Article
em En
| MEDLINE
| ID: mdl-21295458
ABSTRACT
A hallmark event in neurodegenerative diseases is the accumulation of misfolded aggregated proteins in the brain leading to neuronal dysfunction and disease. Compelling evidence suggests that misfolded proteins damage cells by inducing endoplasmic reticulum (ER) stress and alterations in calcium homeostasis. Changes in cytoplasmic calcium concentration lead to unbalances on several signaling pathways. Recent data suggest that calcium-mediated hyperactivation of calcineurin (CaN), a key phosphatase in the brain, triggers synaptic dysfunction and neuronal death, the two central events responsible for brain degeneration in neurodegenerative diseases. Therefore, blocking CaN hyper-activation might be a promising therapeutic strategy to prevent brain damage in neurodegenerative diseases.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Estresse Fisiológico
/
Doenças Neurodegenerativas
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Calcineurina
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Retículo Endoplasmático
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Deficiências na Proteostase
Limite:
Animals
/
Humans
Idioma:
En
Revista:
Curr Opin Cell Biol
Ano de publicação:
2011
Tipo de documento:
Article
País de afiliação:
Estados Unidos