ArticleFrontiers in immunology2026
Deciphering the regulatory mechanism and therapeutic potential of ECM degradation in intervertebral disc degeneration via multi-omics integration.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Intervertebral disc degeneration (IVDD) is a major cause of chronic low back pain, characterized not only by extracellular matrix (ECM) degradation but also by a chronic low-grade inflammatory response. The crosstalk between immune microenvironment dysregulation and protease-driven ECM breakdown remains poorly understood, hindering the development of targeted therapies. Methods: We integrated multiple transcriptomic datasets to map the landscape of ECM-degrading proteases in IVDD. Machine learning algorithms (LASSO, Random Forest, SVM) were employed to identify key regulatory genes. Their association with immune cell infiltration and inflammatory pathways was investigated. A diagnostic ridge regression model was constructed, and molecular docking was performed to screen for potential therapeutics. The top candidate, pravastatin sodium, was validated Results: MMP3 and ADAMTS1 were identified as core genes driving ECM degradation, and their expression was strongly correlated with the abundance of pro-inflammatory immune cells and activation of inflammatory pathways. The model based on these genes effectively distinguished degenerated discs. Single-cell analysis revealed that high-degradation nucleus pulposus cells exhibited enhanced pro-inflammatory intercellular communication and metabolic reprogramming towards a pro-inflammatory state. Molecular docking confirmed high binding affinity of pravastatin sodium to MMP3 and ADAMTS1. Experimental validation demonstrated that pravastatin sodium alleviated IVDD by reducing ECM degradation, suppressing pro-inflammatory cytokine (e.g., IL-1β) expression, and inhibiting apoptosis. Conclusion: Our study delineates a critical network linking ECM degradation to immune microenvironment activation in IVDD, with MMP3 and ADAMTS1 serving as central hubs. Pravastatin sodium emerges as a promising therapeutic agent capable of disrupting this pathogenic network, offering a novel immunomodulatory strategy for slowing disc degeneration.
Indexed as
Identifiers
What Socratic holds
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.