ArticleAging cell2025
BRD4/MAP2K7/PGF Signaling Axis Promotes Senescence and Extracellular Matrix Metabolism of Nucleus Pulposus Cells in Intervertebral Disk Degeneration.
Article in Aging cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Wogonin Ameliorates the Oxidative Stress, Apoptosis, and Extracellular Matrix Degradation of Nucleus Pulposus Cells Mediated byInternational journal of molecular sciences · 2026Article
- A ROS and pH dual - responsive hydrogel-nanoparticle system restores intervertebral disc and alleviates related pain by modulating senescence and panoptosis of nucleus pulposus cells.Materials today. Bio · 2026Article
- Fargesin enhances the condition of intervertebral disc degeneration by suppressing BRD4 expression and influencing autophagy in NPCs.Journal of molecular histology · 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
- Resetting the epigenetic clock: cellular senescence and regenerative strategies in intervertebral disc degeneration.Frontiers in aging · 2026Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Intervertebral disk degeneration (IDD) is a common age-related degenerative disease of the spine that imposes a substantial economic burden on both families and society. Despite substantial advances in understanding the mechanisms underlying IDD, effective therapeutic interventions for its treatment and prevention remain elusive. Our previous study identified a positive correlation between IDD severity and bromodomain-containing protein 4 (BRD4) expression. However, the multifaceted role of BRD4 in IDD is still not fully understood. This study explored the abnormal elevation of BRD4 expression in nucleus pulposus (NP) tissues from patients with IDD and in an age-related rat model of IDD. We found that BRD4 levels were positively correlated with NP senescence and extracellular matrix (ECM) degradation and inversely correlated with ECM anabolism. These relationships were further confirmed through assays measuring senescence-associated β-galactosidase activity, the expression of senescence markers P21 and P16, senescence-associated secretory phenotype indicators (IL-6, IL-8, MMP3, and MMP13), as well as ECM metabolism markers such as collagen II and aggrecan. Mechanistically, aberrant BRD4 expression was found to upregulate MAP2K7, which in turn enhances PGF expression, promoting NP cell senescence and ECM metabolism. These findings highlight the crucial role of the BRD4/MAP2K7/PGF signaling axis in cellular senescence and ECM regulation, suggesting that BRD4 represents a promising therapeutic target for IDD.
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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 Socratic graph.