ArticleBone research2025
Fibrocyte enrichment and myofibroblastic adaptation causes nucleus pulposus fibrosis and associates with disc degeneration severity.
Article in Bone research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Biomaterials for intervertebral disc regeneration: Niche reprogramming, precision therapeutics, and structural reconstruction.Bioactive materials · 2027Review
- Versatile Microgel Platform for Intervertebral Disc Degeneration Therapy: Targeting Pericyte-Mediated Fibrosis and Protecting Nucleus Pulposus Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Single-cell multi-omics defines H3K27me3 remodelling in intervertebral disc degeneration with implications for regenerative intervention.Bone research · 2026Article
- Surviving the Nucleus Pulposus Desert: Next-Generation Strategies for Intervertebral Disc Cell Therapy.JOR spine · 2026Article
- Integrated bioinformatics, single-cell analysis, and experimental validation identify quercetin as a potential therapeutic candidate for intervertebral disc degeneration.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Biomaterial-based strategies targeting ferroptosis for alleviating intervertebral disc degeneration: Advances and perspectives.Journal of orthopaedic translation · 2026Review
- Integrative bulk and single-cell transcriptomic analyses reveal nucleus pulposus cell fibrosis as a therapeutic target in intervertebral disc degeneration and identify quercetin as a potential antifibrotic agent.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Integrative analysis of single-cell RNA sequencing, bulk RNA sequencing, and proteomic data identified NOTCH3 as a hub gene contributing to human intervertebral disc fibrosis.Scientific reports · 2026Article
- Understanding the Microenvironment of Intervertebral Disc Degeneration: A Comprehensive Review of Pathophysiological Insights and Therapeutic Implications.International journal of molecular sciences · 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
- Role of oxidative stress in intervertebral disc degeneration: mechanisms, pathogenesis, and therapeutic strategies.Molecular biology reports · 2025Review
- Article
- Nanomedicine Approaches for Intervertebral Disc Regeneration: From Bench to Bedside.Pharmaceutics · 2025Review
- Mechanisms of prostatic inflammation-mediated male lower urinary tract symptoms.American journal of clinical and experimental urology · 2025Review
Corrections and comments
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibrotic remodeling of nucleus pulposus (NP) leads to structural and mechanical anomalies of intervertebral discs that prone to degeneration, leading to low back pain incidence and disability. Emergence of fibroblastic cells in disc degeneration has been reported, yet their nature and origin remain elusive. In this study, we performed an integrative analysis of multiple single-cell RNA sequencing datasets to interrogate the cellular heterogeneity and fibroblast-like entities in degenerative human NP specimens. We found that disc degeneration severity is associated with an enrichment of fibrocyte phenotype, characterized by CD45 and collagen I dual positivity, and expression of myofibroblast marker α-smooth muscle actin. Refined clustering and classification distinguished the fibrocyte-like populations as subtypes in the NP cells - and immunocytes-clusters, expressing disc degeneration markers HTRA1 and ANGPTL4 and genes related to response to TGF-β. In injury-induced mouse disc degeneration model, fibrocytes were found recruited into the NP undergoing fibrosis and adopted a myofibroblast phenotype. Depleting the fibrocytes in CD11b-DTR mice in which myeloid-derived lineages were ablated by diphtheria toxin could markedly attenuate fibrous modeling and myofibroblast formation in the NP of the degenerative discs, and prevent disc height loss and histomorphological abnormalities. Marker analysis supports that disc degeneration progression is dependent on a function of CD45
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