ArticleCell death discovery2025
NOXA exacerbates endoplasmic-reticulum-stress-induced intervertebral disc degeneration by activating apoptosis and ECM degradation.
Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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.
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Who cites it
3 citing papers in PubMed.
- Exosomes derived from senescent skeletal muscle cells aggravate nucleus pulposus cell metabolic dysregulation via p38MAPK pathway for promoting intervertebral disc degeneration.BMC musculoskeletal disorders · 2026Article
- DDRGK1 preserves intervertebral disc development through ufmylation.Cellular and molecular life sciences : CMLS · 2025Article
- Kallikrein-kinin system as a potential target for the treatment of intervertebral disc degeneration.European journal of medical research · 2025Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Intervertebral disc degeneration (IVDD) is a prevalent condition leading to low back pain. Endoplasmic reticulum stress (ERS) is strongly linked to IVDD progression, although the underlying mechanisms remain unclear. In this study, we investigated the effects of NOXA on ERS-induced IVDD. Primary nucleus pulposus cells (NPCs) were stimulated with Thapsigargin to mimic the ERS microenvironment in IVDD. Western blot analysis, PCR, immunofluorescence, and immunohistochemistry assay were performed to measure the expression levels of PERK, NOXA, and cell apoptosis- and extracellular-matrix-degradation-relevant proteins. JC-1 fluorescent probes, terminal deoxynucleotidyl transferase dUTP nick end labeling staining, and flow cytometry were used to measure mitochondrial function and apoptosis in NPCs under ERS conditions. Magnetic resonance imaging, Safranin O staining, alcian blue staining, and immunohistochemistry were performed to estimate the effects of NOXA knockdown on acupuncture-mediated IVDD in rats at both imaging and histological levels. The results showed that ERS induced and activated the PERK pathway during IVDD development. Mechanically, ERS induced NPC apoptosis and ECM degradation by upregulating PERK expression and activating NOXA expression. The genetic overexpression of NOXA inhibited cell proliferation and increased apoptosis, whereas its knockdown decreased MCL-1 expression and alleviated IVDD degeneration in human NPCs and rat models. NOXA plays a crucial role in the PERK/NOXA/MCL-1 axis, mediating the link between ERS and IVDD. Targeting NOXA expression may be an effective method for treating IVDD, laying the foundation for future research on molecular mechanisms and the development of new therapies.
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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.