Interplay between ER stress and autophagy: A possible mechanism in multiple sclerosis pathology.
Exp Mol Pathol
; 108: 183-190, 2019 06.
Article
em En
| MEDLINE
| ID: mdl-31047874
ABSTRACT
Multiple sclerosis (MS) is a chronic autoimmune inflammatory disease of the central nervous system that results in demyelination, neurodegeneration, and axonal loss. During MS pathology, autoreactive T cells specific for self-antigens migrate the blood-brain-barrier and are responsible for the axonal and neuronal damage. ER stress, a disruption in cellular homeostasis due to the accumulation of misfolded proteins, is a hallmark of MS pathology. In response to the homeostatic imbalance, ER stress activates the unfolded protein response, an intricate system of signaling pathways that aims to restore cellular balance. During the UPR, various autophagy pathways are also activated. Autophagy is a diverse network of regulatory catabolic processes which direct the clearance of damaged and unnecessary organelles and proteins while recycling necessary cellular components. In respect to its role in the health of the immune system, autophagy is critical to the survival and proliferation of T cells. This review consolidates current knowledge and recent literature about ER stress, UPR, and autophagy in MS and implicate their crosstalk as a characteristic feature of MS, potentially aiding in the development of novel therapeutic strategies for MS research.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Autofagia
/
Estresse do Retículo Endoplasmático
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Esclerose Múltipla
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Neurônios
Tipo de estudo:
Prognostic_studies
Limite:
Animals
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Humans
Idioma:
En
Revista:
Exp Mol Pathol
Ano de publicação:
2019
Tipo de documento:
Article
País de afiliação:
Estados Unidos