ArticleOxidative medicine and cellular longevity2021
The Role of Unfolded Protein Response in Human Intervertebral Disc Degeneration: Perk and IRE1-
Article in Oxidative medicine and cellular longevity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
22 citing papers in PubMed, 23 citations in OpenAlex.
- Article
- Stress-response exhaustion in intervertebral disc degeneration.Frontiers in cell and developmental biology · 2026Review
- Navigating Cellular Stress: Endoplasmic Reticulum Stress and the Unfolded Protein Response in the Molecular Pathogenesis of Preeclampsia.Cell biochemistry and biophysics · 2025Review
- Exosomal miR-221-3p derived from bone marrow mesenchymal stem cells alleviates endoplasmic reticulum stress-mediated apoptosis in nucleus pulposus cells via the Nrf2/HO-1 signalling pathway.International journal of experimental pathology · 2025Article
- A Cross-Tissue Transcriptome-Wide Association Study Identified Susceptibility Genes for Intervertebral Disc Degeneration.JOR spine · 2025Article
- Review
- Endoplasmic Reticulum-Dependent Apoptotic Response to Cellular Stress in Patients with Rheumatoid Arthritis.International journal of molecular sciences · 2025Article
- Do wolframin, P-glycoprotein, and GRP78/BiP cooperate to alter the response of L1210 cells to endoplasmic reticulum stress or drug sensitivity?Cancer cell international · 2025Article
- Lipid metabolic disorders and their impact on cartilage endplate and nucleus pulposus function in intervertebral disk degeneration.Frontiers in nutrition · 2025Review
- Druggable Genome-Wide Mendelian Randomization Identifies Distinct Therapeutic Targets for Low Back Pain, Intervertebral Disk Degeneration, and Sciatica.Journal of pain research · 2025Article
- miR-1275 Delivered via Mesenchymal Stem Cell-Derived Extracellular Vesicles Regulates ER-Phagy Through AXIN2 in Nucleus Pulposus Cells.Stem cells international · 2025Article
- LRP1 mitigates intervertebral disc degeneration by inhibiting endoplasmic reticulum stress through stabilizing the PPARγ.Journal of orthopaedic translation · 2025Article
- IRE1α pathway: A potential bone metabolism mediator.Cell proliferation · 2024Review
- Gene Expression Profiling to Unfolded Proteins Response as a Risk Modulator of Patients with Rheumatoid Arthritis.International journal of molecular sciences · 2024Article
- Insights into the underlying pathogenesis and therapeutic potential of endoplasmic reticulum stress in degenerative musculoskeletal diseases.Military Medical Research · 2023Review
- Engineered extracellular vesicles as therapeutics of degenerative orthopedic diseases.Frontiers in bioengineering and biotechnology · 2023Review
- Comprehensive analysis of senescence-related genes and immune infiltration in intervertebral disc degeneration: a meta-data approach utilizing bulk and single-cell RNA sequencing data.Frontiers in molecular biosciences · 2023Article
- Panax notoginseng saponin reducesAnnals of translational medicine · 2022Article
- RETREG1-mediated ER-phagy activation induced by glucose deprivation alleviates nucleus pulposus cell damage via ER stress pathway.Acta biochimica et biophysica Sinica · 2022Article
- Endoplasmic reticulum stress associates with the development of intervertebral disc degeneration.Frontiers in endocrinology · 2022Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammation plays a key role in intervertebral disc degeneration (IDD). The association between inflammation and endoplasmic reticulum (ER) stress has been observed in many diseases. However, whether ER stress plays an important role in IDD remains unclear. Therefore, this study is aimed at investigating the expression of ER stress in IDD and at exploring the underlying mechanisms of IDD, ER stress, and inflammation. The expression of ER stress was activated in nucleus pulposus cells from patients who had IDD (D-NPCs) compared with patients without IDD (N-NPCs); and both the proliferation and synthesis capacity were decreased by inducer tunicamycin (Tm) and proinflammatory cytokines. Pretreatment of NPCs with 4-phenyl butyric acid (4-PBA) prevented the inflammatory cytokine-induced upregulation of unfolded protein response- (UPR-) related proteins and recovered cell synthetic ability. Furthermore, proinflammatory cytokine treatment significantly upregulated the expression of inositol-requiring protein 1 (IRE1-
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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.