RETREG1-mediated ER-phagy activation induced by glucose deprivation alleviates nucleus pulposus cell damage via ER stress pathway

• DOI: 10.3724/abbs.2022024
• Publication Date: 2022-05-16T15:15:21Z
• Authors: Rongjin Luo; Huaizhen Liang; Weifeng Zhang; Gaocai Li; Kangcheng Zhao; Wenbin Hua; Yu Song; Cao Yang
• Keywords: 0303 health sciences; senescence; ER-phagy; Nucleus Pulposus; intervertebral disc degeneration; apoptosis; Apoptosis; QD415-436; Intervertebral Disc Degeneration; QH426-470; Endoplasmic Reticulum; Endoplasmic Reticulum Stress; Biochemistry; 03 medical and health sciences; Glucose; Genetics; Autophagy; Humans; ER stress

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.