RETREG1-mediated ER-phagy activation induced by glucose deprivation alleviates nucleus pulposus cell damage via ER stress pathway.
Acta Biochim Biophys Sin (Shanghai)
; 54(4): 524-536, 2022 Apr 25.
Article
em En
| MEDLINE
| ID: mdl-35607959
ABSTRACT
Accumulating evidence indicates that ER-phagy serves as a key adaptive regulatory mechanism in response to various stress conditions. However, the exact mechanisms underlying ER-phagy in the pathogenesis of intervertebral disc degeneration remain largely unclear. In the present study, we demonstrated that RETREG1-mediated ER-phagy is induced by glucose deprivation (GD) treatment, along with ER stress activation and cell function decline. Importantly, ER-phagy was shown to be crucial for cell survival under GD conditions. Furthermore, ER stress was suggested as an upstream event of ER-phagy upon GD treatment and upregulation of ER-phagy could counteract the ER stress response. Therefore, our findings indicate that RETREG1-mediated ER-phagy activation protects against GD treatment-induced cell injury via modulating ER stress in human nucleus pulposus cells.
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Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Degeneração do Disco Intervertebral
/
Núcleo Pulposo
Limite:
Humans
Idioma:
En
Revista:
Acta Biochim Biophys Sin (Shanghai)
Ano de publicação:
2022
Tipo de documento:
Article