ArticleJournal of translational medicine2025
SOX4 accelerates intervertebral disc degeneration via EZH2/NRF2 pathway in response to mitochondrial ROS-dependent NLRP3 inflammasome activation in nucleus pulposus cells.
Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Biomaterials for intervertebral disc regeneration: Niche reprogramming, precision therapeutics, and structural reconstruction.Bioactive materials · 2027Review
- Article
- Edaravone-based precision antioxidative therapy alleviates intervertebral disc degeneration via the Nrf2/Aldh3a1 axis.Materials today. Bio · 2026Article
- Efficacy and Mechanisms of Duhuo Jisheng Decoction in Treating Intervertebral Disc Degeneration: A Network Pharmacology and Experimental Study.Current medical science · 2026Article
- TEAD4 and RXRA Regulate the Function of Nucleus Pulposus Cells in Intervertebral Disc Degeneration Via the TNF-α/NF-κB Pathway: An Integrated Analysis of Single-Cell RNA-Seq, Bulk RNA-Seq, and In Vitro Validation.Applied biochemistry and biotechnology · 2026Article
- DDIT3 drives nucleus pulposus cell PANoptosis and intervertebral disc degeneration progression.Apoptosis : an international journal on programmed cell death · 2026Article
- Rebuilding the degenerative disc microenvironment: mesenchymal stem cells, exosomes, and bioengineered scaffolds.Frontiers in bioengineering and biotechnology · 2026Review
- miR-188-5p accelerates intervertebral disc degeneration by mediating P4HB to regulate ferroptosis in nucleus pulposus cells.European journal of medical research · 2025Article
- Apoptotic Pathway in Intervertebral Disc Degeneration: From Molecular Pathways to Clinical Interventions.Diagnostics (Basel, Switzerland) · 2025Review
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Authors and funding
4 authors.
Funding
Abstract
objectiveThe transcription factor SRY-related HMG-box 4 (SOX4) has been implicated in intervertebral disc diseases. This study aimed to investigate the role of SOX4 in intervertebral disc degeneration (IDD) and explore the underlying molecular mechanisms.
methodsWe established an IDD rat model via surgery and analyzed SOX4 expression using qRT-PCR and Western blotting. Histological evaluation, immunohistochemistry, and Safranin O staining assessed IDD progression. In vitro, an IDD cellular model was constructed using IL-1β-stimulated nucleus pulposus (NP) cells. SOX4 knockdown and overexpression experiments in NP cells examined SOX4 effects on ECM degradation, NLRP3-mediated pyroptosis, and mitochondrial ROS-dependent NLRP3 inflammasome activation. The involvement of the EZH2/NRF2 pathway in SOX4-mediated NLRP3 activation was also examined.
resultsSOX4 expression was significantly increased in IDD rats and promoted IDD progression. Knockdown of SOX4 inhibited ECM degradation and NLRP3-mediated pyroptosis in NP cells. In vitro experiments showed that SOX4 promoted ECM degradation by upregulating MMPs and ADAMTS-5 expression, and suppressed collagen II and aggrecan synthesis. SOX4 knockdown inhibited NLRP3-mediated pyroptosis, while overexpression accelerated it in NP cells. Additionally, SOX4 was found to exacerbate mitochondrial ROS-dependent NLRP3 inflammasome activation in NP cells. Further investigation revealed that SOX4 enhanced NLRP3 inflammasome activation by upregulating EZH2 expression and modulating the EZH2/NRF2 pathway, with EZH2 inhibition attenuating SOX4-induced NLRP3 activation.
conclusionOur findings suggest that SOX4 accelerates IDD progression by promoting NLRP3 inflammasome activation via modulating the EZH2/NRF2 pathway, leading to NP cell pyroptosis and ECM degradation. Targeting SOX4 may represent a potential therapeutic strategy for treating IDD.
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