ReviewSmart medicine2026
Organ-on-a-Chip Technology: Advances in Modeling Inflammation, Neurovascularization and Nociception in Human Intervertebral Disc Degeneration.
Review in Smart medicine, 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
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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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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.
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0 citing papers in PubMed.
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
An organ-on-a-chip platform has emerged as an advanced in vitro model that replicates organ-level structures within physiologically relevant human microenvironments. In this review, we focus on intervertebral disc (IVD) degeneration, a leading cause of chronic low back pain, providing a comprehensive overview of the current understanding of IVD anatomy, physiology, and pathogenesis. We review conventional in vitro, ex vivo, and in vivo models, which have expanded our understanding; however, they inadequately reproduce the human phenotype, heterogeneous disc composition and anatomy, which comprises nucleus pulposus (NP) and annulus fibrosus (AF) with neovascularization and sensory innervation within the three-dimensional (3D) degenerative microenvironment. We emphasize a disc-on-a-chip platform to address these limitations, which integrates microfluidics and biomimetic ECM-based hydrogels within a controlled microenvironment to miniaturize the disc. It offers a promising platform to simulate the pathological disc milieu by incorporating gradient control of key signaling molecules implicated in disc degeneration. These include a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) and matrix metalloproteinase (MMP)-mediated extracellular matrix (ECM) degradation; tumor necrosis factor alpha (TNF-α) and interleukin-1 beta (IL-1β)-driven inflammation via nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB); vascular endothelial growth factor (VEGF)-promoted angiogenesis; and nerve growth factor (NGF)- and brain-derived neurotrophic factor (BDNF)-mediated sensory innervation and sensitization, thus contributing to nociception. Collectively, disc-on-a-chip offers a next-generation in vitro model for investigating mechanisms relating to ECM degradation, inflammation, innervation, vascularization, and nociception underlying IVD degeneration, enabling precision preclinical therapeutic evaluations.
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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 OpenQuestion graph.