ArticleScientific reports2026
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.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
The trial behind it
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Who cites it
1 citing paper in PubMed.
- ITGBL1 and RPN1 Mark a Fibrotic NP Subpopulation with Coupled Integrin Signaling and N-Glycosylation Programs in IVDD.Journal of inflammation research · 2026Article
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intervertebral disc degeneration (IDD) is marked by nucleus pulposus (NP) fibrosis, but its molecular drivers remain unclear. This study investigated NP cellular heterogeneity and key regulators using integrative multi-omics. NP specimens from IDD patients and controls were analyzed by scRNA-seq, bulk RNA-seq, proteomics, and fibrosis histological staining. Bioinformatics identified NP subtypes, pseudotime trajectories, and intercellular communication. Validation included immunostaining, qRT-PCR, Western blotting, and functional assays following NOTCH3 knockdown or over-expression. Fibrosis staining confirmed increased collagen deposition in degenerated NP tissues. scRNA-seq revealed eight NP subpopulations, with fibroblast-like NP cells enriched in degeneration. Degenerated samples showed enhanced NOTCH, IGF, and TGF-β signaling. Multi-omics consistently identified NOTCH3 as a hub gene. Functional experiments showed NOTCH3 promoted apoptosis, senescence, fibroblast differentiation, and ER stress–associated fibrosis, while silencing reversed these effects. Immunohistochemistry confirmed elevated NOTCH3 in degenerated tissues. NOTCH3 is a central regulator of NP fibrosis and degeneration, acting via ER stress and fibrotic pathways. Targeting NOTCH3 may represent a novel therapeutic strategy for restoring disc homeostasis in IDD.
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Registered trials
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