ArticleActa biochimica et biophysica Sinica2022
RETREG1-mediated ER-phagy activation induced by glucose deprivation alleviates nucleus pulposus cell damage via ER stress pathway.
Article in Acta biochimica et biophysica Sinica, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- RETREG1-Mediated Reticulophagy is Essential for Dendritic Cell Maturation and Function in Sepsis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Stress-response exhaustion in intervertebral disc degeneration.Frontiers in cell and developmental biology · 2026Review
- Unveiling ER-Phagy Receptors in Thyroid Cancer: A Combined Approach of Public Data Mining and In Vitro Validation.Clinical Medicine Insights. Oncology · 2026Article
- Inhibition of Endoplasmic Reticulum Stress Cooperates with SLC7A11 to Promote Disulfidptosis and Suppress Tumor Growth upon Glucose Limitation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Nucleus pulposus cells regulate macrophages in degenerated intervertebral discs via the integrated stress response-mediated CCL2/7-CCR2 signaling pathway.Experimental & molecular medicine · 2024Article
- Insights into the underlying pathogenesis and therapeutic potential of endoplasmic reticulum stress in degenerative musculoskeletal diseases.Military Medical Research · 2023Review
- Alterations of bovine nucleus pulposus cells with aging.Aging cell · 2023Article
- Rosuvastatin suppresses TNF-α-induced matrix catabolism, pyroptosis and senescence via the HMGB1/NF-κB signaling pathway in nucleus pulposus cells.Acta biochimica et biophysica Sinica · 2023Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.