ArticleArchives of medical science : AMS2026
Metformin alleviates intervertebral disc degeneration by upregulating MMP-1 expression via the KDM6A/SOX9/miR-202-3p/MMP-1 signaling pathway.
Article in Archives of medical science : AMS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
- Resetting the epigenetic clock: cellular senescence and regenerative strategies in intervertebral disc degeneration.Frontiers in aging · 2026Review
- Recent Advances in Managing Spinal Intervertebral Discs Degeneration.International journal of molecular sciences · 2022Review
- The effects of rivaroxaban, an oral anticoagulant, on human IVD primary cultures.Archives of medical science : AMS · 2022Article
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Authors and funding
3 authors.
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Abstract
Introduction: MiR-202-3p is involved in the pathogenesis of intervertebral disc degeneration (IDD) via regulating MMP-1 expression in neuronal precursor cells (NPCs). As an activator of miR-202-3p and KDM6A expression, metformin (MET) may regulate the expression of SOX9 via regulating the methylation status of the SOX9 promoter. However, the role of MET in the treatment of IDD remains to be explored. Material and methods: Quantitative real-time PCR was performed to analyze the expression of KDM66, SOX9, MMP-1 and miR-202-3p in NPCs and IDD rabbits. Western blot was carried out to evaluate the expression of KDM6A, SOX9 and MMP-1 protein under different conditions. Bisulfite sequencing PCR was used to analyze the DNA methylation of the SOX9 promoter. Luciferase assay was carried out to explore the inhibitory effect of miR-202-3p upon MMP-1. Results: The expression of KDM6A, SOX9 and MMP-1 was abnormal in IDD cells and rabbits, while the MET treatment restored the normal expression of KDM6A, SOX9 and MMP-1 and miR-202-3p. Mechanistically, MET treatment reduced the level of hypermethylation of the SOX9 promoter, thus restoring the expression of SOX9 in IDD cells and rabbits. The elevation in SOX9 expression promoted the expression of miR-202-3p, therefore inhibiting the expression of MMP-1, a downstream target of miR-202-3p. Conclusions: In this study, we set up cellular and animal models of IDD and treated them with MET to probe the effect of MET on IDD and the signaling pathway of KDM6A/SOX9/miR-202-3p/MMP-1. Our work provided deep insight into the molecular mechanism underlying the therapeutic role of MET in the treatment of IDD.
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