Simon Y. Tang

This paper develops a microfluidic platform to model sensory neuron-intervertebral disc crosstalk by combining biochemical and electric-field stimulation.

This study shows that modulating RAGE through genetic or pharmacologic means can reverse diabetes-induced bone impairments across multiple scales.

This study tracks the temporal changes in chemokine production and neurovascular invasion in mouse intervertebral discs during degeneration following injury.

This study examines the transcriptome and secreted factors in intervertebral discs of STZ-HFD T2D mice, revealing increased inflammation and degeneration compared to controls.

This study uses single-cell RNA sequencing to analyze changes in cell function and maturation in the intervertebral disc after injury, identifying key cell populations and pathways involved in degeneration.

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 examines how RAGE signaling and Type 2 Diabetes affect cortical bone mechanics, structure, and material properties in mice, showing sex-specific improvements with RAGE ablation.

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