ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Human iPSCs Derived MSCs-Secreted Exosomes Modulate Senescent Nucleus Pulposus Cells Induced Macrophage Polarization via Metabolic Reprogramming to Mitigate Intervertebral Disc Degeneration.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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
14 citing papers in PubMed.
- Biomaterials for intervertebral disc regeneration: Niche reprogramming, precision therapeutics, and structural reconstruction.Bioactive materials · 2027Review
- MSC-EVs in Cartilage Regeneration and Immunomodulation: Mechanisms and Therapeutic Prospects for Osteoarthritis, Rheumatoid Arthritis and Intervertebral Disc Degeneration.International journal of molecular sciences · 2026Review
- Surviving the Nucleus Pulposus Desert: Next-Generation Strategies for Intervertebral Disc Cell Therapy.JOR spine · 2026Article
- Macrophage Lipid Homeostasis Drives IVDD via a Senescence-Dependent Impairment of Efferocytosis.Cell proliferation · 2026Article
- Review
- A manganese-luteolin co-loaded antioxidant hydrogel for synergistic alleviation of oxidative stress and immunomodulation in intervertebral disc degeneration.Materials today. Bio · 2026Article
- TDP43 cytoplasmic mislocalization initiates mitochondrial dysfunction and intercellular senescence propagation in intervertebral disc degeneration.Experimental & molecular medicine · 2026Article
- Immunometabolism: A Novel Therapeutic Target and Its Pharmacological Modulation for Intervertebral Disc Degeneration.International journal of molecular sciences · 2026Review
- Rebuilding the degenerative disc microenvironment: mesenchymal stem cells, exosomes, and bioengineered scaffolds.Frontiers in bioengineering and biotechnology · 2026Review
- Mesenchymal stem cell and exosome-based therapies for degenerative disc disease: from mechanisms to clinical translation.Frontiers in cell and developmental biology · 2026Review
- Resetting the epigenetic clock: cellular senescence and regenerative strategies in intervertebral disc degeneration.Frontiers in aging · 2026Review
- Regenerative Potential of Extracellular Vesicles on Intervertebral Disc Degeneration: What is the EV-idence?JOR spine · 2025Review
- Human iPSCs Derived MSCs-Secreted Exosomes Modulate Senescent Nucleus Pulposus Cells Induced Macrophage Polarization via Metabolic Reprogramming to Mitigate Intervertebral Disc Degeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Integrating multi-omics and machine learning to explore the role of amino acid metabolism in intervertebral disk degeneration.Frontiers in neurologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
Intervertebral disc degeneration (IDD) is a leading cause of discogenic lower back pain, yet the crosstalk between macrophage polarization and nucleus pulposus (NP) cell senescence in IDD progression remains poorly understood. Emerging therapies using human induced pluripotent stem cell (iPSCs)-derived mesenchymal stem cells (iMSCs) show promise for IDD treatment. In this study, it is first demonstrated that senescent NP cells promote macrophage polarization toward the pro-inflammatory M1 phenotype in coculture systems. Reciprocally, conditioned medium from M1 macrophages exposed to senescent NP cells accelerates senescence in healthy NP cells. Notably, it is identified that iMSCs-derived exosomes break this pathogenic cycle by reprogramming M1 macrophages toward anti-inflammatory M2 phenotypes. Mechanistically, these exosomes deliver miR-100-5p to suppress mTORC1 signaling and regulate glycolysis metabolic reprogramming in macrophages. These findings are corroborated in a rat IDD model, where iMSC-exosomes mitigate IDD progression in vivo. This work elucidates a novel iMSC-exosomes mediated mechanism regulating macrophage-NP cell interactions, which provides a promising therapeutic strategy for IDD intervention.
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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.