Spine and Intervertebral Disc Pathology

This study shows that PDGF-AB/BB treatment reduces senescence in human intervertebral disc cells by modulating gene expression related to cell cycle, metabolism, and oxidative stress.

This study shows HMGB1 promotes macrophage recruitment and worsens intervertebral disc degeneration after injury, with knockout mice showing reduced mechanical and structural damage.

This study shows that VEGFA drives neurovascular invasion in degenerating intervertebral discs and contributes to chronic low back pain, with its inhibition preventing pain behaviors.

This study examines intervertebral disc (IVD) impairments in a mouse model of Alzheimer's Disease, finding no increased degeneration but altered mechanical properties and volume.

This study establishes a rat model of lumbar spine instability through intervertebral disc injury and evaluates musculature adaptations.

The paper analyzes mineral phase changes in intervertebral discs from dogs, finding that herniated discs contain crystalline hydroxyapatite while non-herniated discs have amorphous calcium phosphate.

This study identifies SM/J mice as a model for spontaneous disc herniations and shows neuroimmune changes drive chronic discogenic pain.

This study identifies TNFR1-mediated senescence and limited TNFR2 signaling as barriers to intervertebral disc cell repair in back pain, suggesting immunomodulation as a therapeutic strategy.

This study integrates single-cell RNA sequencing and WGCNA to identify chondrocyte subtypes, hub genes, and inflammatory pathways in intervertebral disc degeneration.

This study shows that lactate transfer via MCT1 between nucleus pulposus and endplate cells is essential for intervertebral disc health, as its absence leads to degeneration.

The paper uses a Parallel Network methodology to predict TIMP and protease activity in NP cells under various mechanical and inflammatory conditions.

This study shows oral K3Citrate reduces disc calcification in LG/J mice without affecting bone structure or locomotion, suggesting Ca2+ chelation as a potential mechanism.

The paper develops a regulatory network model of nucleus pulposus cells to simulate ECM regulation in intervertebral discs, showing how perturbations affect catabolic and anabolic processes.

This study conducts a genome-wide meta-analysis across three biobanks to identify new genetic loci associated with lumbar disc herniation, expanding the known genetic landscape.

This study identifies sex-specific immune cell responses following intervertebral disc injury, revealing differential recruitment of gamma-delta T cells in female mice and NKT cells in males.

This study shows that SIRT6 loss in mice leads to intervertebral disc degeneration by promoting senescence and SASP through changes in histone modifications, DNA accessibility, and autophagy.

This study compares muscle force changes in different spinal stenosis surgeries using musculoskeletal modeling, finding that laminotomy reduces muscle compensation compared to laminectomy.

The paper identifies a stress-induced subtype of nucleus pulposus cells in degenerating intervertebral discs that trigger discogenic low back pain.

The paper generates and compares single-cell atlases of human neonatal and adult intervertebral discs to identify cellular heterogeneity, sub-populations, and developmental trajectories.

This paper describes a biobank protocol for studying lumbar disc degeneration using clinical and omics data from 1100 participants.

The paper identifies altered biological processes and signaling pathways in stretched nucleus pulposus cells using transcriptomic analysis of a rat dataset.

This study identifies miR-31-5p as a key regulator of intervertebral disc degeneration, showing it promotes cell proliferation, inhibits apoptosis, and reduces matrix degradation by targeting the SDF-1/CXCR7 axis.

DIPPER provides a spatiotemporal proteomics atlas of human intervertebral discs, revealing region-specific regulatory profiles and a hydration matrisome linked to MRI intensity.

This paper develops a hybrid Agent-based model to simulate intervertebral disc cell behavior in 3D multifactorial environments, showing cell death and viability changes under simulated stress conditions.

This study identifies ADGRG6 as a regulator of intervertebral disc homeostasis through STAT3 signaling, showing that inhibiting STAT3 reduces disc degeneration in a mouse model.

The paper uses polygenic scores to show genetic overlaps between lumbar disc degeneration and height, BMI, and BMD in Chinese and Japanese cohorts.